Ciências Fisiológicas

URI Permanente desta comunidade

http://repositorio.ufes.br/handle/10/17570

Programa de Pós-Graduação em Ciências Fisiológicas

Centro: CCS
Telefone: (27) 3335 7340
URL do programa: http://www.cienciasfisiologicas.ufes.br/pt-br/pos-graduacao/PPGCF

Navegar

Agora exibindo 1 - 20 de 343

A disfunção ventricular direita pós-infarto do miocárdio está associada com o desenvolvimento da insuficiência cardíaca
(Universidade Federal do Espírito Santo, 2010-05-07) Fernandes, Aurélia Araújo; Zornoff, Leonardo Antônio mamede; Stefanon, Ivanita; Alessandra Simao Padilha; Vassallo, Dalton Valentim; Pereira,Fausto Edmundo Lima
Heart failure (HF) is the major cause of death and morbidity after myocardial infarction (MI) that can result in reduced cardiac output, increased venous pressure and cardiac remodeling. Usually, the left ventricle failing causes right dysfunction being related to greater risk of hospitalization. It has been suggested that assessment of right ventricle (RV) function is of important value to prognostic of HF after MI. Therefore, the aim of this study was to assess right ventricle contractility early (one week) and late phase (eight weeks) after MI. MI with signal of HF (HF group) and without signal of HF (Inf group) were compared to a sham-operated group (sham). Wistar male rats were anaesthetized with Ketamine (50 mg/kg) and Xylazine (5 mg/kg), i.m., and MI was induced through left coronary artery ligation at 3 mm of its origin. After 1 and 8 weeks the rats was anaesthetized with urethane (1.2 g/kg i.p.) and a catheter was inserted into the aorta and left ventricle to pressures measurements using a pressure transducer (TSD 104A) coupled to a Biopac MP100 system. Strips from the right ventricle were removed and attached to an isometric transducer and superfused at 30ºC with Krebs solution, stimulated at 0.5 Hz and 80 mV. The experimental protocols were approved by the local animal ethics committee (CEUA-EMESCAM). Both infarct groups presented same scar size (Inf 1 week= 32.4 ± 3; HF 1 week=33.7 ± 2.2; Inf 8 weeks= 26.5 ± 1.1; HF 8 weeks= 25 ± 0.9). The scar size did not have correlation with HF signals (left ventricle end diastolic pressure (LVEDP), increased lung weight and body weight ratio (LW/BW) and right ventricle to body weight ratio (RV/BW) neither with RV contractility. The LVEDP increased in HF group but not in the Inf group early (1 week: HF=15 ± 1*; Inf=5.2 ± 0.8; Sham=3,7 ± 0,6 mmHg) and late after MI (8 weeks: Hf=16 ± 2.5*, Inf- 7.5 ± 0.7; Sham= 5.2 ± 0.8 mmHg), *P< 0.05 ANOVA one way, post hoc Tukey. In the HF group LW/BW and RV/BW ratio was increased in the late phase, but not in the early phase after MI. The body weight was smaller in the HF group at 1 week, but similar to sham 13 and Inf 8 weeks after MI. Therefore, there was a negative correlation between force development in the RV strips and body weight in both early and late phase after MI. The inotropic responses to Ca2+ and Isoproterenol were preserved in HF group one week after MI and reduced at 8 weeks (8 weeks; CaCl2 2.5 mM: sham= 157 ± 18.4; Inf= 138 ± 17.3; HF= 62 ± 10.3 g/g P<0.05; Isoproterenol 10- 5 M: sham = 149 ± 14; Inf = 137 ± 18.7; HF = 58 ± 8.1 g/g P<0.05). Inversely, in the Inf group, the positive intropic response was reduced in the early phase and reduced in the late phase (1 week; CaCl2 2.5 mM: Sham= 186 ± 8.3; Inf = 135 ± 11.7; HF= 158 ± 13.1 g/g; P<0.05; Isoproterenol 10-5 M: Sham= 145 ± 9.9; Inf= 108 ± 10.8; HF= 166 ± 12 g/g P<0.05). The Ca2+ handling proteins expression (sarcoplasmatic reticulum calcium pump (SERCA-2a), phosfolamban (PLB total), PLB phosphorylated and Na+ /Ca2+ exchange) were not different among the groups in the early phase. But, in the late phase there was a SERCA-2a overexpression and an higher SERCA/PLB ratio just in the Inf group. In conclusion, the scar size did not correlate with HF signals neither with RV contractility. The RV dysfunction was found in the late phase after MI in rats with HF. However, the rats with HF maintain the RV function in early phase after MI. The infarct rats without HF maintained the RV contractility and increase SERCA-2a expression in the late phase after MI. The different inotropic βadrenergic response between the groups with and without HF could be induced by different mechanisms involving upregulation and downregulation of the βreceptors during the early and late phase after MI.
A estimulação transcraniana por corrente contínua aguda impacta o desempenho de jogadores de futebol? Um estudo observacional controlado duplo cego
(Universidade Federal do Espírito Santo, 2022-09-16) Rocha, Jader Vinicius da Silva; Arêas, Fernando Zanela da Silva; https://orcid.org/0000-0002-2068-2606; http://lattes.cnpq.br/2219697069216192; https://orcid.org/0000-0001-9978-165X; http://lattes.cnpq.br/8889080992224610; Barauna, Valerio Garrone; https://orcid.org/0000000328320922; http://lattes.cnpq.br/1583882564447423
The search for increased performance and physical performance are linked to the use of ergogenic resources. The vertical jump is one of the measures commonly used to evaluate the performance of lower limbs in athletes. Transcranial direct current stimulation (tDCS) is a noninvasive, safe, economically viable technique that can modulate cortical excitability, which can influence the increase in the performance of athletes in general. The aim of this study was to investigate whether the use of tDCS on the motor cortex (M1) results in an improvement in the performance of soccer players. This is a cross-sectional study where 27 players were randomized into three groups: Active tDCS group (n=9); Sham group (n=9) and control group (n=9). Stimulation was applied at an intensity of 2 mA for 15 minutes using a bi-hemispheric cephalic mount. Athletes performed the vertical jump before and after tDCS. The subjects' heart rate (HR) was monitored before and after the vertical jump. After the jump, the subjective perception of effort (RPE) was recorded. Visual pain scale (VAS) and subjective recovery scale (RPE) were monitored before and after tDCS. No differences were found in any of the performance variables analyzed (p > 0.05) nor in the responses of HR (p > 0.05), PSE (p > 0.05), VAS (p > 0.05) and EPR (p > 0.05) between groups. The tDCS in M1 did not change the performance of the vertical jump and there was no improvement in the subjective scales. Additionally, new studies should be developed with stimulus intensities in different cortical areas and different sports modalities.
A exposição aguda a alta concentração de cobre prejudica a contratilidade miocárdica: participação das espécies reativas de oxigênio
(Universidade Federal do Espírito Santo, 2018-04-13) Filetti, Filipe Martinuzo; Vassallo, Dalton Valentim; Simões, Maylla Ronacher; Santos, Leonardo dos; Fioresi, Mirian
Copper is an essential metal for homeostasis and the functioning of living organisms, but in overload can lead to systemic harmful effects. Copper toxicity can be related to reactive oxygen species (ROS) production and cardiovascular diseases. We testing the effects of high copper concentration (10 μg/mL) on the myocardial mechanics, investigating the ROS-mediated effects. The developed force of papillary muscles was reduced after acute exposure to high copper and prevented by co-incubation with tempol, DMSO and catalase. The indirect evaluation of sarcoplasmic reticulum activity was reduced by copper and restored by tempol. The contractile response to calcium was reduced by copper and reversed by antioxidants. The response to β-adrenergic agonist decreased after exposure to copper and restored by tempol and catalase. Contractions dependent on the sarcolemmal calcium influx were impaired by copper and restored by antioxidants. In addition, in situ detection in papillary muscles showed increased O2 •- and OH• . The myosin-ATPase activity decreased significantly. In conclusion, high copper concentration can acutely impair myocardial excitationcontraction coupling reducing the capacity to generate force, by reducing calcium inflow and of its reuptake, myosin-ATPase activity, and these effects are mediate by local production of O2 •- , OH• and H2O2. These toxicity effects suggest that exposure to high copper concentration is a risk factor for cardiovascular disease
A exposição crônica ao chumbo diminui a reatividade vascular em aorta de ratos: papel do peróxido de hidrogênio
(Universidade Federal do Espírito Santo, 2014-12-17) Nunes, Karolini Zuqui; Fioresi, Mirian; Vassallo, Dalton Valentim; Gouvea, Sonia Alves; Moyses, Margareth Ribeiro; Peçanha, Giulia Alessandra Wiggers
We investigated whether exposure to small concentrations of lead alters blood pressure and vascular reactivity.Wistar rats were sorted randomly into the following two groups: control (Ct) and treatment with 100 ppm of lead (Pb), which was added to drinking water, for 30 days. Systolic blood pressure (BP) was measured weekly. Following treatment, aortic ring vascular reactivity was assessed. Tissue samples were properly stored for further biochemical investigation. The lead concentration in the blood reached approximately 8 µg/dL. Treatment increased blood pressure and decreased the contractile responses of the aortic rings to phenylephrine. Following LNAME administration, contractile responses increased in both groups but did not differ significantly between them. Lead effects on Rmax were decreased compared to control subjects following superoxide dismutase administration, Catalase, DETCA, and apocynin increased the vasoconstrictor response induced by phenylephrine in the aortas of lead-treated rats but did not increase the vasoconstrictor response in the aortas of untreated rats. TEA potentiated the vasoconstrictor response induced by phenylephrine in aortic segments in both groups, but these effects were greater in lead-treated rats. The co-incubation of TEA and catalase abolished the vasodilatory effect noted in the lead group. The present study is the first to demonstrate that blood lead concentrations well below the values established by international legislation increased blood pressure and decreased phenylephrine-induced vascular reactivity. The latter effect was associated with oxidative stress, specifically oxidative stress induced via increases in hydrogen peroxide levels and the subsequent effects of hydrogen peroxide on potassium channels.
A Exposição Crônica e Baixas Doses de Cloreto de Mercúrio Altera a Reatividade Vascular da Artéria Aorta de Ratos. Papel das Espécies Reativas do Oxigênio e dos Prostanóides da Via da Ciclooxigenase .
(Universidade Federal do Espírito Santo, 2009-05-07) Pecanha, Franck Maciel; Vassallo, Dalton Valentim; Stefanon, Ivanita; Pereira, Fausto Edmundo Lima; Cibin, Francielli Weber Santos
Mercury exposure produces toxic effects in central nervous system and kidneys. Recently these toxic effects were associated to cardiovascular events but the underlying mechanisms are not well explored. The main purpose of this study was to investigate if mercury exposure at low doses alters vasoconstrictor prostanoids production from cyclooxygenase-2 (COX-2) and its contribution to phenylephrine vasoconstrictor responses and acetylcholine vasodilator responses. For this were developed an experimental model of exposure to low doses of mercury chloride (HgCl2) and evaluated the effect of this exposure on systolic blood pressure (SBP), the participation of products derived from the endothelium, prostanoids derived from the cyclooxygenase-2 (COX-2), reactive oxygen species (ROS) and the reninangiotensin system in vascular reactivity in conductance arteries. Aortic segments from 3-month old Wistar rats daily treated with HgCl2 (1st dose 4.6 µg/kg, subsequent dose 0.07 µg/kg/day, i.m) or vehicle for 30 days were used. The vascular reactivity experiments were performed in an organ bath, the atomic absorption spectrometry for determination of blood concentration of mercury, RT-PCR and Western blot to verify the gene and protein expression, confocal microscopy analyzed levels of superoxide anion and structure of arteries. A commercial kit used to determine the production of prostanoids derived from COX-2 pathway. The activity of angiotensinconverting enzyme (ACE) was measured by fluorometry method and SBP by tail plethysmography. Blood levels of mercury at the end of treatment were 7.97 ± 0.59 ng/ml. Mercury treatment did not affect systolic blood pressure, but increased phenylephrine contractile responses, reduced acetylcholine-induced vasodilatation and did not change the vasodilatation by the nitric oxide donor, DEA-NO, in aortic rings. The contractile prostanoids derived from COX-2 pathway, reactive oxygen species (ROS) and increased plasmatic ACE activity were related to these responses. Increased production of EROS, increased plasma ACE activity, increased gene expression of mRNA for COX-2 and increased production of contractile prostanoids (PGE2 and TXA2) derived from COX-2 were observed in animals exposed to mercury and reinforce the hypothesis of a greater involvement of these pathways in the alteration of vascular response to phenylephrine. In the presence of superoxide dismutase (SOD) the vasodilator response to acetylcholine was improved in rats of the mercury group, indicating that endothelial dysfunction appears to be responsible for the increased production of EROS. The extracellular SOD (EC-SOD) expression was increased by exposure to mercury. These results suggest that this new experimental model of chronic exposure at low concentrations of HgCl2 promotes endothelial dysfunction due to the reduced bioavailability of NO induced by increased oxidative stress, and increase the contractile response to phenylephrine with greater involvement of the reninangiotensin system, EROS and contractile prostanoids derived from COX-2 pathway in this response. These results help to clarify the mechanisms by which mercury at low doses exerts toxic effects on the cardiovascular system and can be considered a risk factor for development of cardiovascular disease.
A exposição única ao contaminante ambiental tributilestanho induz disfunção endotelial e estresse oxidativo em aorta
(Universidade Federal do Espírito Santo, 2018-09-27) Santos, Gersica de Almeida Correia; Ribeiro Júnior, Rogério Faustino; Stefanon, Ivanita; Andrade, Tadeu Uggere de; Rodrigues, Lívia Carla de Melo
INTRODUCTION: Organotins such as tributyltin (TBT) are environmental contaminants with a cytotoxic effect. Animals chronically exposed to TBT have vascular reactivity dysfunction associated with increased production of reactive oxygen species (ROS). The aim of this study was to investigate the effect of a single exposure to TBT. Vascular reactivity of isolated female rat aorta rings was evaluated 24 hours after exposure to a single dose of TBT (500 ng / kg) per gavage. METHOD: Wistar rats (240-260 g) were divided into control (CT) groups, and exposed to a single dose of TBT. The aorta was isolated and cut into rings, which were immersed in Krebs solution submitted to the concentration response curve of phenylephrine, LNG-nitroarginine methyl ester (L-NAME), Apocynine, Tiron and Losartan. The vasodilatory response was assessed by relaxing the increasing doses of Acetylcholine (ACh). In addition, the presence of ROS was measured by the intensity of the fluorescence produced by the oxidation of the dihydroetide (DHE). Data were expressed as mean ± SEM and analyzed by 2-way ANOVA or unpaired t-test with significance of p <0.05. The protocols were approved by the Ethics Committee on Animal Experimentation UFES (Protocols 27/2016). RESULTS: The aortic rings from the TBT group showed reduction of sensitivity (pD2) and the maximum response (Rmax) to ACh (pD2 TBT: 6.37 ± 0.27 * vs CT: 7.3 ± 0.25; Rmax TBT: 77 ± 5,18 * vs. CT: 92.9 ± 1.88 *, * p <0.05 vs CT), and increased maximal response and phenilefrine sensitivity (Rmax: TBT: 142 ± 7.2 ** vs CT : 110 ± 4% KCl, ** p <0.01; pD2: TBT: 7.68 ± 0.08 * vs. CT: 7.19 ± 0.13% KCl, * p <0.05 vs. CT). A incubation of the aortic rings with L-NAME increased the reactivity to phenilefrine in both groups (Rmax TBT: 142.2 ± 7.2 vs TBT L-NAME: 175 ± 7.8 # and CT: 110 ± 4 vs. CT LNAME: 165 , 7 ± 8.6 **% KCl, # p <0.05 vs TBT, ** p <0.01 vs CT). However, the area under the curve (dAUC %) was lower in the TBT vs CT group (CT: 52.4 ± 4.61 vs TBT: 35.8 ± 4.31 * p <0.05). The maximum response to phenilefrine was reduced in the TBT group after incubation with Apocinin, Tiron, Catalase and Losartan (TBT: 142 ± 7.2 vs TBT APO: 102.9 ± 5.42 # # TBT TIRON: 104.3 ± 9, TBT: 101.8 ± 7.38 % KCl; # # p <0.01 vs TBT). ROS was increased in the aorta of the animals exposed to TBT. CONCLUSION: We conclude that 24 hours after exposure to a single dose of 20 500 ng / kg TBT causes endothelial dysfunction, increase in the vasoconstrictor response to phenylephrine and a reduction in the vasodilatory response to acetylcholine that appears to be mediated by vascular oxidative stress.
A Influência dos hormônios sexuais no balanço entre as citocinas pró-inflamatórias e anti-inflamatórias em machos e fêmeas SHR, após o tratamento com enalapril
(Universidade Federal do Espírito Santo, 2011-12-16) Dalpiaz, Polyana Lima Meireles; Moyses, Margareth Ribeiro; Bissoli, Nazaré Souza; Gouvea, Sonia Alves; Garcia, Ana Raquel Santos de Medeiros
Introduction: Angiotensin II, a peptide formed from the action of angiotensin converting enzyme (ACE) on angiotensin I, is a primary mediator of the reninangiotensin system (RAS) and in addition to hemodynamic effects, is involved in key events the inflammatory process. The use of ACE inhibitors, apart from hemodynamic benefits, is associated with anti-inflammatory effects, however, still unclear whether ACE inhibitors have beneficial effects on the balance between pro-and anti-inflammatory cytokines and hormones can interfere with this relationship. Thus, this study was designed to investigate in SHR rats, males and females, castrated and intact, the potential benefit of ACE inhibitors on serum levels of inflammatory biomarkers, IL-10, IL-6 and TNF-α, since that these cytokines play important roles in the pathogenesis of inflammatory diseases. Objective: To evaluate the influence of gender on the effect of enalapril on serum levels of proinflammatory cytokines (IL-6 and TNF-α) and antiinflammatory (IL-10) in SHR rats. Methods: SHR, adults, both sexes, with 12 weeks, weight 150 ± 8 g (females) and 230 ± 10 g (males), were separated into eight experimental groups (n = 7) are: Males and Females 1) SHAM + Treatment with vehicle, 2) SHAM + treatment with enalapril, 3) castration + treatment with enalapril, 4) castration + treatment with vehicle. Treatment by gavage with enalapril (10mg/kg/day) was started after 21 days of castration and lasted 4 weeks. Sham group animals underwent sham surgery group and the castrated animals, underwent bilateral ovariectomy and orchidectomy, males and females respectively. We analyzed the plasma ACE activity of the cytokines IL-10, IL-6 and TNF-α. Level of significance: p <0.05. Results: Enalapril reduced SBP and ACE activity in all treated groups, we observed sexual dimorphism in plasma levels of IL-10, TNF-α and IL-6 in the sham groups, with higher values in females. The withdrawal of sex hormones made disappear the difference between males and females in relation to inflammatory cytokines and reversed the pattern of response. Enalapril treatment increased IL-10 in all treated groups, thus improving the balance proand anti-inflammatory, regardless of gender. Conclusion: The neutralization of the actions of angiotensin II by ACE inhibitors in SHR may exert anti-inflammatory and anti-hypertensives, regardless of sex, but dependent on sex hormones to reduce pro-inflammatory cytokines.
A ingestão elevada de frutose altera a reatividade vascular mesentérica em ratos normotensos
(Universidade Federal do Espírito Santo, 2017-02-17) Sousa, Glauciene Januário de; Bissoli, Nazaré Souza; Baldo, Marcelo Perim; Gouvêa, Sônia Alves; Nogueira, Breno Valentim
Chronic metabolic diseases are a common outcome of modern western lifestyle, as shown by the current prevalence of as obesity, insulin resistance and metabolic syndrome (MS), which correlates with increased fructose consumption and can leads to cardiovascular diseases. We hypothesize that high intake of chronic fructose mimics the early stages of cardiometabolic disease like to the MS, leading to initial vascular alterations. Methods: Wistar rats was separated in tow groups: (FRU) fructose 10% in drink water for 6 weeks and (CON) without fructose. Blood pressure was evaluated by tail plethysmography. Fasting glucose, insulin and glucose tolerance test was made using a strip-based glucometer. Mesenteric vascular beds reactivity was tested in a perfused system. Western blot analysis of iNOS, eNOS, Nox2 and COX-2 was performed. DHE stain was used to vascular O2 - detection. Scanning electron microscopy provided ultrastructural vessel observation. Results: Blood pressure was no altered. FRU shown increased visceral fat deposition and liver weight as well as increased fasting glucose and impaired insulin and glucose tolerance. Fructose increased NEinduced vasoconstriction which was abolished by both indomethacin and endothelium removal. ACh-induced relaxation was preserved, and L-NAME promoted a significant reduction in response in the FRU group. The SNP-induced relaxation was not altered. Protein expression of iNOS was increased, however, there was no changes in the eNOS, Nox2 and COX-2. DHE shown no differences. Additionally, the scanning electron microscopy images showed a slight disarray in the endothelium layer surface that are suggestive of derangement of the intima layer with a change in the shape and arrangement of the endothelial cells. Conclusions: High fructose intake for 6 weeks leads to metabolic disturbance and promotes increased NOR-induced vasoconstriction through endothelial prostaglandins pathway as well as increased the NO-mediated relaxation associated with iNOS increase.
A inibição da DPP-4 previne a disfunção vascular induzida pela hiperatividade β-adrenérgica
(Universidade Federal do Espírito Santo, 2018-08-10) Oliveira, Bruna Coelho de; Santos, Leonardo dos; Barauna, Valério Garrone; Santos, Roger Lyrio dos; Campos, Luciene Cristina Gastalho; Caceres, Viviane de Menezes
The increase in sympathetic activity is involved with the genesis and maintenance of disease states that affect the cardiovascular system. Β-adrenergic hyperactivity induces the formation of local inflammatory factors in vascular tissue, leading to vascular dysfunction. A possible pharmacological strategy of controlling vascular injury by the inflammatory process is to inhibit the enzyme dipeptidyl peptidase-4. DPP-4 inhibitors are of the class of drugs used to treat type 2 diabetes mellitus by increasing the half-life of GLP- 1 and improve glycemic control. We aimed to test the hypothesis that the DPP-4 inhibitor reverses vascular dysfunction and attenuates the inflammatory process caused by β-adrenergic hyperactivity. Male Wistar rats (Rattus norvegicus) weighing between 300 and 350g were used. The animals were randomly divided into three groups: vehicle group (VHC), isoproterenol (non-selective βadrenergic agonist) (ISO) and isoproterenol group plus sitagliptin (DPP-4 inhibitor) (ISO + SITA). A human umbilical vein endothelial cell line (EAhy.926) and primary vascular smooth muscle cells (VSMC), obtained by the explant method of the thoracic aorta of wistar rats, were used. We have shown in our results that isoproterenol caused cardiac hypertrophy of 28% and sitagliptin was not able to prevent this response. There was no change in cardiorespiratory function. Inhibition of DPP-4 was able to prevent the increase in the contractile response to phenylephrine, in addition, it prevented the endothelial dysfunction caused by isoproterenol in vascular reactivity, observed by the mechanical removal of the endothelium. Chronic treatment with isoproterenol did not alter DPP-4 activity, but increased mRNA expression of the proinflammatory cytokines IL-1β (86%), IL-6 (45%) and MCP-1 (84%) in the aorta , while sitagliptin reduced to baseline. In vitro, isoproterenol did not alter the activity of DPP-4 and the expression of inflammatory cytokines in VSCV, but increased the activity of DPP-4 and inflammatory cytokines in endothelial cells (IL-1β, 49%, IL-6, 39%; MCP-1, 43%) and sitagliptin reduced to baseline. In conclusion, our study demonstrated that inhibition of DPP-4 by sitagliptin improves vascular dysfunction and significantly attenuates endothelial inflammation in an experimental model of β-adrenergic hyperactivity.
A PRIVAÇÃO ANDROGÊNICA DE LONGO PRAZO MODULA A REATIVIDADE VASCULAR POR VIAS DEPENDENTES DE ALDOSTERONA E ANGIOTENSINA II
(Universidade Federal do Espírito Santo, 2022-08-31) Costa, Anna Karolina Nascimento; Stefanon, Ivanita; https://orcid.org/0000-0003-2638-5183; http://lattes.cnpq.br/8456612999765726; https://orcid.org/; http://lattes.cnpq.br/0575590472541198; Bissoli, Nazare Souza; https://orcid.org/; http://lattes.cnpq.br/8865368585732583; Davel, Ana Paula Couto; https://orcid.org/; http://lattes.cnpq.br/
Testosterone is a vasoactive hormone, which acts by genomic and non-genomic mechanisms. Acutely, it may have endothelium-dependent vasodilatory actions. However, the long-term modulation of testosterone on the regulation of vascular tone remains unclear. The hypothesis of this study is that, in the long term, testosterone participates in the vascular reactivity regulation, dependent on the renin-angiotensin- aldosterone system. Wistar rats (N=128), at 12 weeks of age, were divided into male Control (SHAM) and orchiectomy surgery (OQT), treated for 3 months with losartan, an angiotensin II receptor blocker (SHAM+LOS and OQT+ LOS), 15 mg/kg, s.c); spironolactone (SHAM+SPI and OQT+SPI, 80 mg/kg, gavage), mineralocorticoid receptor antagonist and apocynin, NADPH oxidase inhibitor (SHAM+APO and OQT+APO, 30 mg/kg, drinking water), Vascular reactivity was analysed in isolated aortic rings, as the percentage of response to KCl (75 mM), superfused with modified Krebs pH 7.4, 36.5oC. The presence of vascular presence was observed in vitro as curves-response to phenylephrine (10-11 to 10-3 M) and absence of: L-NAME, 100 μM; indomethacin (INDO, 10 μM) and endothelium-denuded rings (E-). Plasma lipid peroxidation was measured using the TBARS technique. (CEUA-UFES 017/2020). Results were expressed as mean ± SEM and using Student's t test, analysis of variance (ANOVA), one way. The OQT groups, untreated and OQT treated with APO and LOS, had lower body weight at the end of the 3 months (SHAM 231 ± 11g; OQT= 158,4 ± 13,0g*; OQT+APO 208,3 ± 15,4g; OQT+LOS 156,0 ± 23,0g *p<0,05). The Rmax for phenylephrine was the same between the SHAM and OQT groups. Treatments for 3 months with LOS and APO did not change Rmax to phenylephrine. However, LOS treatment reduced the pD2 of the OQT group (log EC50: OQT= -6.240 ± 0.15 vs OQT+LOS= -7.218 ± 0.23 *p<0.01). Inhibition of MR receptors with spironolactone determined a lower maximal contraction to phenylephrine in the OQT group than in the SHAM, suggesting that this pathway could be testosterone dependent. (SHAM+SPI =120.4 ± 7.56% n=10 vs OQT+SPI= 93.3 ± 10.2% n=10; *p<0.05). Phenylephrine reactivity increased in the presence of L-NAME and in the absence of E, similarly between the groups. Inhibition of the COX pathway with indomethacin determined a reduction in Rmax in both groups (Rmax SHAM= 118.3 ± 8.04 vs SHAM+INDO = 56.27 ± 6.61, p <0.01 and OQT= 119.8 ± 8.41 vs OQT+INDO= 72.64 ± 9.34, p<0.01). There was no difference in reactivity between the groups incubated with indomethacin (SHAM+INDO and OQT+INDO). There was a reduction in RMax, in the presence of indomethacin, only in the OQT+SPI group. This result suggests the participation of aldosterone in the COX activation pathway, possibly of a vasoconstrictor, since in the SHAM+SPI group, indomethacin reduced the maximum contraction (Rmax: SHAM+SPI = 120.4 ± 7.56; OQT+ SPI= 93.28 ± 10.18; SHAM+SPI+INDO = 89.99 ± 8.45; OQT+SPI+INDO = 74.15 ± 7.92, * p <0.05). Endothelial NO bioavaliability seems to have been modified in the group treated with losartan, especially in the OQT+LOS- LN group, suggesting the importance of the testosterone pathway in the production of NO mediated by angiotensin II receptors. These data suggest that testosterone participates in the production of NO mediated by angio II, because when we remove the production of NO, through the LN, in the OQT group, there was a reduction in Rmax in relation to its control. Is suggests the importance of testosterone in the contractile response. mediated by the AT1 angiotensin receptor (Rmax: SHAM+LOS = 127.5 ± 5.63; OQT+LOS = 135.6 ± 4.74; SHAM+LOS LN = 183.4 ± 10.50; OQT+LOS LN = 151.8 ± 8.311; * p<0.05). The effects of treatment with the angiotensin II inhibitor, losartan, on rings without endothelium, showed that the endothelium injury caused an increase in the response to phenylephrine in the SHAM group. However, there was no difference between the OQT+LOS E- and OQT+LOS CT groups, suggesting a vasoconstrictor positive modulation that depends on the presence of angiotensin II. These data suggest that testosterone participates in the production of NO mediated by angio II, because when we remove the production of NO, through the LN, in the castrated group there is a reduction in Rmax in relation to its control, suggesting the importance of testosterone in the contractile response. mediated by the AT1 angiotensin receptor (Rmax: SHAM+LOS = 127.5 ± 5.63; OQT+LOS = 135.6 ± 4.74; SHAM+LOS LN = 183.4 ± 10.50; OQT+LOS LN = 151.8 ± 8.311; * p<0.05). The effects of treatment with the angiotensin II inhibitor, losartan, on rings without endothelium, showed that the endothelium injury caused an increase in the response to phenylephrine in the SHAM group. However, there was no difference between the OQT+LOS E- and OQT+LOS CT groups, suggesting a vasoconstrictor positive modulation that depends on the presence of angiotensin II. Orchidectomy modified the endothelium-dependent response during treatment with losartam (Rmax: SHAM+LOS = 127.5 ± 5.63; OQT+LOS = 135.6 ± 4.74; SHAM+LOS E- = 217.3 ± 217.3 ± 26.77; OQT+LOS E- = 145.3 ± 7.90. * p<0.05). In conclusion, the set of these results suggest the long term participation of testosterone and aldosterone in the modulation of vascular contraction induced by phenylephrine.
A terapia com células mononucleares atenua a aterosclerose em camundongos ApoE Knockout
(Universidade Federal do Espírito Santo, 2011-12-12) Porto, Marcella Leite; Meyrelles, Silvana dos Santos; Vasquez, Elisardo Corral; Baldo, Marcelo Perim; Errera, Flávia Imbroisi Valle
Cardiovascular diseases are leading causes of morbidity and mortality worldwide. Among these, there is atherosclerosis, a chronic inflammatory disease of the arterial wall. Despite conventional therapies (pharmacological or surgical interventions) are of great value, cell therapy emerges as a new therapeutic strategy for treating and preventing atherosclerosis. Thus, the aim of this study was to evaluate the effects of mononuclear cell (MNC) therapy on the development of atherosclerotic lesions in the apolipoprotein E knockout (apoE KO) mouse. ApoE KO female mice (24-week-old) were randomly divided into two groups: 1) an apoE KO control group (n = 8) and 2) an apoE KO group that received MNC therapy (apoE KO-MNC, n = 8). β-galactosidase (β-gal) (encoded by the lacZ gene) transgenic mice (12-week-old) were used as MNC donors. Six-month-old apoE KO mice were fed a cholesterol-rich diet (1.25% cholesterol) for 4 to accelerate the process of atherogenesis. ApoE KO-MNC received mononuclear cells isolated from the spleen of lacZ mice (106 cells / week) for 8 weeks. After euthanasia, a blood sample was collected and the plasma total cholesterol was measured. The aorta was removed for immunohistochemical analysis. We investigated vascular lipid deposition, vascular remodeling, oxidative stress, endothelial nitric oxide synthase (eNOS) expression and the presence of endothelial progenitor cells. in apoE KO mice treated with spleen MNCs isolated from lacZ transgenic mice (apoE KO-MNC) compared to untreated control mice (apoE KO). Data are presented as the mean ± SEM. Statistical analysis was performed with Student’s t-test for independent samples or one-way analysis of variance (ANOVA). Statistical significance was set at p < 0.05. Histological analysis of aortas showed a significant reduction in the lipid deposition area in apoE KO-MNC mice compared to apoE KO mice (0.051 ± 0.004 vs 0.117 ± 0.016 mm2, respectively, p < 0.01). In addition, vessel morphometry revealed that MNC therapy prevented the outward (positive) remodeling in apoE KO mice that is normally observed (apoE KO-MNC: 0.98 ± 0.07 vs apoE KO: 1.37 ± 0.09), using wildtype mice (C57BL/6J) as a reference. ApoE KO-MNC mice also have reduced 15 production of superoxide anions and increased eNOS expression compared to apoE KO mice. Finally, immunohistochemistry analysis revealed a homing of endothelial progenitor cells (EPCs) in the aortas of apoE KO-MNC mice. We concluded that MNC therapy attenuates the progression of atherosclerosis in the aortas of apoE KO mice. Our data provide evidence that the mechanism by which this attenuation occurs includes the homing of EPCs, a decrease in oxidative stress and an upregulation of eNOS expression.
AÇÃO DO TRATAMENTO COM KEFIR NA REATIVIDADE VASCULAR DE RATAS OVARIECTOMIZADAS
(Universidade Federal do Espírito Santo, 2020-06-26) Couto, Mariana dos Reis; Bissoli, Nazare Souza; https://orcid.org/; http://lattes.cnpq.br/8865368585732583; https://orcid.org/; http://lattes.cnpq.br/; Biancardi, Vinicia Campana; https://orcid.org/; http://lattes.cnpq.br/; Santos, Roger Lyrio dos; https://orcid.org/; http://lattes.cnpq.br/1122196233280741
Studies have shown that estrogen contributes to the proper functioning of the cardiovascular system, since it can modulate the generation of relaxation and contraction factors derived from the endothelium. However, in postmenopausal women, the use of horm
Ação moduladora da tibolona no sistema de peptídeos natriuréticos: Implicações cardiovasculares e imunológicas
(Universidade Federal do Espírito Santo, 2010-11-24) Garcia, Ana Raquel Santos de Medeiros; Andrade, Tadeu Uggere de; Bissoli, Nazaré Souza; Reis, Adelina Martha dos; Boechät, Giovanna Assis Pereira; Padilha, Alessandra Simão
Cardiovascular and immune system abnormalities have been reported in females with estrogen deficiency. Nevertheless, the capacity of the exogenous estrogen therapy to manage these hazard effects in postmenopausal women is still to be better investigated. Objective: this study is addressed to determine the abnormalities on the natriuretic peptide system in ovariectomized rats with and without tibolone reposition therapy, and if these changes are or not related with cardiovascular and immunological parameters. Materials and Methods: female rats with the average weight of 160-180 g were used and divided into four groups (n = 7 per group): SHAM, ovariectomized (OVX), OVX treated with 17β-estradiol (EST) and OVX treated with tibolone (TIB). The treatment period was 14 days with TIB (1.5 mg / kg / day) and EST (0.5 mg / kg / day), after 21 days of the ovariectomy procedure. At the end of treatment, the animals were euthanized, the thoracic aorta was isolated, and rings of 4-5 mm were removed. Rings with endothelium, were placed in an isolated organ tank with Krebs solution. Dose-response curves to phenylephrine (PHE) and acetylcholine (ACH) were obtained for assessment of vascular reactivity. Upper segment of the thoracic aorta was used for analysis of protein expression of eNOS by Western Blotting. The kidneys, the atria and blood were collected for further analysis. Plasma levels of atrial natriuretic peptide (ANP) were measured by radioimmunoassay (RIA) and serum cytokines (IL-6 and TNF-α) by ELISA. Atria were removed for analysis by RIA of ANP and atrial ANP mRNA by RT-PCR. The kidneys were used for analysis of mRNA of type A receptor (NPR-A) and C (NPR-C) by RT-PCR. Data were presented as mean ± standard error of mean. Statistical analysis of the reactivity of aortic rings was performed by analysis of variance (ANOVA), and one or two way, followed by post-hoc test of Tukey. For the peptides system data it was performed one-way analysis of variance (ANOVA) followed by post hoc Newman-Keuls, and for eNOS it was used one-way analysis of variance (ANOVA) followed by Fisher's post hoc test. Significance levels were p<0,05. Results: the OVX group showed increase of contractile response to PHE compared to the SHAM group, and the TIB and EST groups were able to normalize this response (Emax - SHAM: 91,0 ± 3,9; OVX: 140,0 ± 5,5; EST: 115,4 ± 3,7; TIB: 113,2 ± 5,1 - % Tension). The endothelium-dependent relaxation (dose-response curves to ACH) was similar for all groups. The OVX, EST and TIB groups showed no difference in the eNOS protein expression compared with the SHAM group, however, serum levels of IL-6 and TNF-α were increased in ovariectomized females. However, the treatments with EST and TIB were able to decrease these levels compared to the SHAM group, except the levels of IL-6 which remained high in the TIB group (TNF-α: SHAM 20.3 ± 2.0, OVX 31.0 ± 5.0, 17.6 ± EST 2.0; TIB: 20.5 ± 3.1 / IL-6: SHAM 19.3 ± 6.0, 32.8 ± 5.0 OVX, EST 20.0 ± 3.0; TIB: 34.4 ± 2.8 pg / ml). The plasmatic and left atrial levels of ANP (ANP plasma: 263.3 ± 53.3 SHAM, OVX 92.5 ± 19.5, 247.3 ± 29.9 EST; TIB: 285.7 ± 60.4 pg / ml / left atrial ANP: SHAM 5.68 ± 0.35; OVX 3.48 ± 0.40, 0.97 ± 6:48 EST; TIB: 3.59 ± 0.25 mg / mg protein), the mRNA expression of ANP left atrial (SHAM 91.3 ± 4.4, OVX 40.0 ± 10.1; 122.3 ± 12.0 EST; TIB: 167.9 ± 25.7 AU) and NPR-A (SHAM 5.20 ± 12:00; OVX 0.68 ± 0.11; EST 0.92 ± 0.28; TIB: 2.04 ± 1.4 AU) were depressed after ovariectomy, and NPRC did not change. The treatment normalized these parameters, except that the TIB group did not normalize the levels of atrial ANP. Conclusion: data from this study show, for the first time, that tibolone treatment after ovariectomy influence the natriuretic peptide system and the inflammatory cytokines. Tibolone was able to normalize the levels of ANP and its atrial expression as well as reduce levels of TNF-α. Additionally, the results show that Hormonal Therapy used in this study partially normalized the changes in vascular reactivity, possibly through regulation of the peptide system and inflammatory cytokines.
Ácido Linoleico Reduz a Reatividade Vascular e Melhora a Disfunção Vascular de Artérias Mesentéricas de Ratos Hipertensos
(Universidade Federal do Espírito Santo, 2018-10-04) Nunes, Dieli Oliveira; Ribeiro Junior, Rogerio Faustino; Padilha, Alessandra Simao; Pereira, Fausto Eduardo Lima; Mill, José Geraldo; Stefanon, Ivanita
Omega-6 polyunsaturated fatty acids are well known for their important role in many physiological functions and in reducing the risks of cardiovascular diseases, especially linoleic acid (LA). Therefore, we aimed to investigate the effect of linoleic acid (LA) treatment on the blood pressure and function of mesenteric resistance arteries (MRA) in spontaneous hypertensive rats (SHR). Male SHR were treated daily with LA (15 mg/kg) or vehicle (control) for 15 days. Compared with controls, LA treatment decreased blood pressure (SBP (mmHg) - Control: 139 ± 1,8 vs LA: 128,4 ± 1,7; DBP (mmHg) - Controle: 78,6 ± 1,1 vs AL: 70,1 ± 3,7 and showed the following in MRA: (1) increased lumen and external diameter, (2) decreased wall:lumen ratio and wall thickness, (3) decreased stiffness and (4) less collagen deposition. LA treatment reduced the contractile response to phenylephrine, although there were no changes observed in MRA in regard to the acetylcholine or sodium nitroprusside responses. Incubation with L-NAME leftshifted the reactivity to phenylephrine only in the MRA treated group, suggesting that LA treatment can improve NO bioavailability, which was confirmed by NO “in situ” quantification analyses. Incubation with tiron decreased vascular reactivity to phenylephrine in MRA in LA rats, which was accompanied by decreased superoxide anion production. Moreover, incubation with indomethacin (nonselective COX inhibitor), NS 398 (COX-2 specific inhibitor), furegrelate (TXA2 synthase inhibitor), SQ 29.548 (TP receptor antagonist) and SC 19220 (EP1 receptor antagonist) reduced the vasoconstrictor responses to phenylephrine in MRA in the treated group. These results were accompanied by a reduction in COX-2 protein expression. In conclusion, these findings show that LA treatment decreases blood pressure, accompanied by structural and functional changes in resistance arteries of SHR rats. These functional changes involve NO bioavailability and reduction in superoxide anion production. At last, the improvement of endothelial dysfunction and structural changes in this hypertension model may be responsible for the reduction in blood pressure.
ÁCIDO ÚRICO SÉRICO EM CRIANÇAS E ADOLESCENTES: DISTRIBUIÇÃO E ASSOCIAÇÃO COM FATORES DE RISCO CARDIOVASCU
(Universidade Federal do Espírito Santo, 2020-03-06) Moulin, Stephanie Rezende Alvarenga; Mill, Jose Geraldo; https://orcid.org/000000020987368X; http://lattes.cnpq.br/2497419234600362; https://orcid.org/; http://lattes.cnpq.br/; Vassallo, Dalton Valentim; https://orcid.org/; http://lattes.cnpq.br/7749285591179880; Sartorio, Carmem Luiza; https://orcid.org/; http://lattes.cnpq.br/1299417616233163; Baldo, Marcelo Perim; https://orcid.org/; http://lattes.cnpq.br/; Cristo, Valeria Valim; http://lattes.cnpq.br/3210373469770019
BACKGROUND: Hyperuricemia in adults is associated with cardiovascular diseases. However, there is lack of information regarding serum uric acid (SUA) determinants in children and adolescents. Our purpose was to determine the SUA distribution in schoolchil
Agentes infecciosos associados à diarréia aguda em crianças até três anos de idade : estudo em um hospital de referência no município de Vitória-ES
(Universidade Federal do Espírito Santo, 2005-10-14) Sadovsky, Ana Daniela Izoton de; Pereira, Fausto Edmundo Lima; Spano, Liliana Cruz; Leite, José Paulo Gagliardi; Morais, Mauro Batista de
Acute diarrhea is one of the main causes of infantile mortality worldwide (WHO), mainly in developing countries. In the present work, the prevalence of Rotavirus (RV), adenovirus (Ad), diarrheogenic E. coli (EPEC, ETEC, EIEC, EHEC, EAEC, DAEC), Salmonella, Shigella, Cryptosporidium spp., Entamoeba histolytica and Giardia lamblia was studied among children up to 3 years old with acute diarrhea. From February 2003 to June 2004, stools samples were obtained prospectly from 253 children with acute diarrhea and 78 without diarrhea attending to the emergency room in a pediatric hospital - Hospital Infantil Nossa Senhora da Glória (HINSG), in Vitória Espírito Santo state, Brazil. Bacterial detection was done in 241 stools samples (12 were excluded because were in use of antimicrobian drugs) and E. coli were isolated in 219 and 68 cases with and without diarrhea, respectively. These cases were submited to serology with policlonal anti-seros (EPEC e EIEC) and hybridization tests (Hybr) to detect virulence genes of EPEC, ETEC, EIEC, EHEC, EAEC e DAEC. RV were studied in 147 cases for immune enzymatic assay (EIARA) and in 230 cases by poliacrylamide gel electrophoresis (PAGE) and Ad, only in 147 cases for immune enzymatic assay (EIARA). Protozoan infection was studied in 88 cases for immune enzymatic assay (EIA). Children with diarrhea were divided in Group I (88 cases = all enteropathogens studied), Group II (147 cases = bacterias, RV e Ad - EIARA) and Group III (230 cases = bacterias and RV - PAGE) and children without diarrhea were Group IV (78 cases = bactérias and RV - PAGE). Enteropathogens were detected in more than 60% in children with acute diarrhea and bacterial infection was the most prevalent: DEC were detected in 41,1%; EPEC in 3,6% (serology) e 9,1% (Hybr); Typical EPEC (0,9%); Atypical EPEC (8,2%); EAEC (9,1%); DAEC (20,6%); EIEC (0,9%); ETEC (4,2%). In stools samples from children without diarrhea, we found Atypical EPEC (10,3%); EAEC (20,6%); DAEC (16,2%); ETEC (1,5%). EHEC was not detected in the studied population. Shigella and Salmonella were detected in 4,6% e 2,9%, respectively, only in children with acute diarrhea. RV were detected in 35,2% (GEPA) and 50% (EIARA); Ad, in 8,2% and E. histolytica, Cryptosporidium spp. and G. lamblia in 8%, 11,4% and 14,8% of cases with diarrhea, respectively. In conclusion, Typical EPEC, EIEC and ETEC were detected only or predominantly in children with acute diarrhea. Atypical EPEC, EAEC and DAEC were not causes of acute diarrhea, except for EAEC in children more than two years old (p = 0,026). RV was the most prevalent agent when the classic enteropathogen DEC (Tipical EPEC, ETEC, EIEC and Shigella e Salmonella) was considered in this study. RV was more frequent in children below 18 months of life and in a period of March, 2003 up September, 2003. Associations among enteropathogens were frequent in the studied population and protozoa were the most of them. Comparing all of protozoa detected, only G. lamblia suggesting being a cause of acute diarrhea, isolately.
Alteraçães ponderais, hemodinâmicas e da função vascular do leito arterial caudal em ratas sete dias após o infarto do miocárdio
(Universidade Federal do Espírito Santo, 2009-01-01) Baldo, Thais de Oliveira Faria; Pereira, Raquel Binda; Stefanon, Ivanita; Vassallo, Dalton Valentim; Pereira, Fausto Edmundo Lima
Infarct area (AI) is an important determinant to heart failure (IC) development. However, studies from our laboratory have been shown that IC nor always correlates with AI. The aim of this study was to evaluate the IC development at 7 days after myocardial infarction (IM), and its consequence on vascular reactivity in the rat tail bed. Female Wistar rats were divided in Control group (CT); fictitious surgery (SHAM); and a group that was submitted to myocardial infarction (INF). Later, the INF group was subdivided in those developed (INFIC) or not (INF) IC. Seven days later, animals were anesthetized and catheterized to assess blood pressure and left ventricular function. After that, the vascular tail bed was removed and perfused under constant flow (2.5 mL/min). Alterations in the mean perfusion pressure (PPM) were acquire after concentration-response curve to phenilephrine (FE, 0.0001-300µg), before and after CHAPS-induced endothelial damage. To evaluate basal nitric oxide (NO) release, L-NAME was used in the presence of FE. To evaluate the dependent or independent relaxation, crescent concentration of acetilcholine (ACh) and sodium nitroprusside (NPS) were perfused after contraction with KCl (65mM). Data are shown as mean ± the standard error of mean, and statistical significance set at P<0.05. Seven days after, animals from INF-IC group showed decreased body weight (PC) (CT: 14.5±2.73; SHAM: 8.14±2.24; INF: - 4.06±2.65; INF-IC: -23.3±4.96g; P<0.05), increased lung/PC ratio (CT: 5.5±0.64; SHAM: 5.5±0.22; INF: 8.44±0.62; INF-IC: 9.90±0.91mg/g; P<0.05) and right ventricle/PC ratio (CT: 0.45±0.03; SHAM: 0.57±0.06; INF: 0.68±0.04; INF-IC: 0.78±0.06mg/g; P<0.05) when compared to other groups. Moreover, increased values for left ventricular end-diastolic pressure (PDFVE) were evidenced in INF-IC group as compared to the others (CT: 1.72±0.8; SHAM: 1.6±0.5; INF: 4.48±0.5; INF-IC: 14.5±1.3mmHg; P<0.05). AI was similar between infarcted groups (INF: 35.8±1.2; INF-IC: 38.8±2.3%; P>0.05). Furthermore, variation in the PC during the seven days correlates with PDFVE (r= -0.592; P<0.05). In the vascular tail bed, INF-IC group showed reduced maximal response (Rmáx) to FE (330.4±13.4 mmHg) as compared to other groups (CT: 423.2±25.4; SHAM: 403.6±28; IM: 425.5±30.4; P<0.05). Basal NO release acquire in the INF-IC group (13.35 ± 2.31) was significantly better as compared to other groups (CT 7.40 ± 1.36; SHAM 7.23 ± 0.8; INF 3.77 ± 0.7; P< 0.05). The relaxation mediated by Ach was reduced in SHAM and INF groups (SHAM: 50.0±2.8; INF: 48.4±2.7 %) as compared to CT and INF-IC groups (CT: 69.1±4.0; INF-IC: 66.9±3.4%; P<0.05). We conclude that seven days after IM is possible to identify animals that, with the same AI, develop or not the IC. Moreover, these animals depict different patterns of vascular response due, at least in part, to a better endothelial NO bioavailability.
Alterações cardiovasculares induzidas pela peçonha da serpente Bothrops leucurus
(Universidade Federal do Espírito Santo, 2018-04-05) Naumann, Gustavo Baptista; Sanchez, Eládio Flores; Figueiredo, Suely Gomes de; Borges, Márcia Helena; Pires, Rita Gomes Wanderley; Gouvêa, Sonia Alves; Bissoli, Nazaré Souza
Bothrops leucurus (white tail jararaca) is the main responsible for ophidian accidents in the northeastern region of Brazil and northern Espírito Santo. Several studies have evaluated the biochemical features of this snake’s venom, as well as its local effects. However, systemic effects – in particular cardiovascular effects – remain rather poorly explored. In the present study, we sought to investigate the acute cardiovascular activities induced by B. leucurus venom (VB) in vivo and in vitro. In anaesthetized rats it was demonstrated that BlV (10-100µg/kg) induces immediate and transient hypotension, while maximum response was observed in 5 min and a return to baseline was observed in ≈ 20 minutes. No change in the heart rate of the animals was observed. In vitro effects were evaluated on pre-contracted mesenteric artery rings with phenylephrine, employing a resistance myograph.
Alterações no perfil proteico do ventrículo esquerdo de ratos após tratamento com óleo de soja: um estudo proteômico
(Universidade Federal do Espírito Santo, 2014-10-03) Soprani, Taisla; Figueiredo, Suely Gomes de; 1º membro da banca
Several studies show that consumption of vegetable oils, such as soybean oil, rich in polyunsaturated fatty acids (PUFAs) has beneficial health effects by preventing or reducing the risk factors of cardiovascular diseases. While the demonstration of the beneficial effects of the consumption of unsaturated fatty acids on the cardiovascular system has been proven in macroscopic level, the molecular/cellular mechanisms responsible for this phenomenon are poorly understood. In this work a comparative proteomic approach, two-dimensional gel electrophoresis (2D) coupled to mass spectrometry (MALDI-TOF / TOF) was applied to investigate the rats heart proteome differences (left ventricle - LV) that not received (control group - CT) and received 0.1mL of soybean oil intramuscularly for 15 days (treated group - TR). Soybean oil treatment induced improvement in left ventricular function, and a significant change in LV proteome in the TR animals. The TR animals present a lower value of LVEDP. The protein profile of VE revealed differences in the expression of 60 protein spots (p<0.05) between CT and TR groups, 14 of these were identified by MS and MS / MS, being 12 non-redundant proteins. Robust changes were detected in proteins involved in muscular contraction, structural and antioxidant system. The TR group presented an increase in intensity of proteins involved in muscle contraction (myosin light chain 3-(3-MCL), creatine kinase M (CKM)) and tireodoxina antioxidant enzyme. Low intensity cytoskeletal protein, desmin, was detected. The differences in the intensity levels of these spots-related proteins in TR group, might be linked to improvement in left ventricular function.
Análise da correlação do espessamento médio-intimal proximal e distal nas carótidas comuns
(Universidade Federal do Espírito Santo, 2011-12-21) Roelke, Leonard Hermann; Mill, Jose Geraldo; França, Luiz Cláudio; Lotufo, Paulo Andrade
Background. The intima-media thickness (IMT) of the carotid arteries has been widely used as a noninvasive method to assess the cardiovascular risk because of its association with ischemic cardiovascular events. In the clinic practice, the IMT has been used as atherosclerosis predictor and as an additional tool to assess the cardiovascular risk according to the Framingham score. The high resolution ultrasound is used to measure carotid IMT in view of superficial localization of the artery and low cost of the exam. Different regions of carotid arteries, however, have been used to assess IMT, going from the common to the internal carotid artery, carotid bulb, either bilaterally or unilaterally. Aims: To correlate the thickening of the media-intima complex in different regions of the common carotid arteries in order to orientate the use of this index in daily clinical practice. Methods: IMT values were measured in the proximal and distal region of both common carotid arteries of 789 participants (both sexes, age 35-74 years) that attended to the Investigation Center of the ELSA study in Espírito Santo State. Images were obtained in the supine position with a Toshiba Aplio (model SSA-790A, version XG) ultrassonography platform by using a large band linear transducer with central frequency of 7.5 MHz (5.0-11.0 MHz). IMT was measured by using the dedicated software of the same equipment. Data were considered as following a normal distribution e the Pearson’s correlation coefficient ( r ) was used to determine the association between the IMT recorded at different sites of right and left common carotid arteries. The analysis were initially performed by the all group and then for the sub-groups without (<0.90 mm, 49% of the sample) a with (≥0.90 mm) subintimal thickening at least at one measured site. Statistical significance of associations was set at p<0.05. Results: A progressive increase in IMT was observed with age in all measured sites in the whole group and associations ranged from 0.56 to 0.69. An important decrease of association ( r ranging from 0.20 to 0.40) was observed in the group IMT≥0.90 mm suggesting low reproducibility of IMT when the thickness of the media-intima complex is increased. Conclusion: Despite the recent recommendations to measure the intima thickening in the distal region of the carotid artery, our data suggest that this recommendation should be restricted to epidemiological studies. The low correlations observed in the ≥0.90 mm group indicate that sub-intimal thickening is a focal process. Therefore, in the clinical practice, the whole extension of both common carotid arteries should be investigated to determine presence of IMT increase

Navegar

Navegando Ciências Fisiológicas por Título

Resultados por página

Opções de Ordenação