Mestrado em Ciências Fisiológicas

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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 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
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 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
Análise das propriedades mecânicas do miocárdio através do plano de fase
(Universidade Federal do Espírito Santo, 2008-05-09) Camilo, Luciana Moisés; Aquino, Regina Maria de; Vassallo, Dalton Valentim; Stefanon, Ivanita; Tucci, Paulo José Ferreira
The phase plane (PP) is a plot of the ventricular pressure in the X-axis and its time derivative in the Y-axis. One of the PP properties is that the final portion is a straight line segment and its slope (Ө) is a time constant that might represent a viscoelastic constant of the muscle. We aimed to compare the behavior of Ө among normal, hypertensives and hypertrophied rat hearts and to evaluate the influences of inotropic interventions on Ө. According an ideal mathematical model of approach of the isovolumic pressure curve, is given that PPA = P x dP/dt. As know that the external cardiac work (Wext) is the time rate of change of work, PdV, the equation can be rewrite in the following way: Text = P. dV . dP dP dt Since in this experimental model the volume is constant, the PPA is proportional to the Wext. The objective of this work was to compare the behavior of Ө and PPA among normal, hypertensives and hypertrophied rats heart and to evaluate the influences of the inotropics interventions on these variables. We used isolated hearts perfused by the Langendorff technique (male Wistar and spontaneously hypertensive rats- SHR), weighing between 210 and 280g, divided in 4 groups: (C) Wistar Control (n=7); SHR (n=7); (ISO,) rats with Isoproterenol-induced hypertrophy (0.3mg/Kg/day, n=9); and (V) rats treated only with vehicle (soyan bean oil, n=6). The experimental protocol consisted of performing ventricular function curves, changes in stimulation frequency and external Ca+2 (0.5, 1.25 and 2.5 mM) and β-adrenergic stimulation (0.1mL; 10- 5M). Left ventricle isovolumic pressure curve and its first derivative (dP/dt) were registered for the construction of the PP. The measures of Ө and PPA were obtained by using the Autocad 2004 software. Results are expressed as mean ± SEM. Statistical analysis: ANOVA 1 and/or 2 way; Fisher post-hoc test, significant for p<0,05. Slopes obtained after stabilization at DP of 10mmHg and during the performance of ventricular function curves were larger in the SHR and ISO groups. 26 The increase of the stimulation frequency significantly increased θ in all groups, as well as the increase of [Ca+2 ex] and the administration of isoproterenol. PPA was higher in SHR group than others. Positive inotropics interventions had provoked proportional increase of PPA in all groups. The increase of the stimulation frequency and the lower [Ca+2 ex] resulted in reduction of the PPA. Myocardial left ventricular hypertrophy in SHR and the chronic treatment with ISO modify the speed of isovolumic pressure decay increasing the slope. Regarding the inotropic interventions the increase of the slope might be linked to the increase of speed of isovolumic pressure decay, due to inotropic action in the helical ventricular myocardial band (HVMB) segments, specifically the ascending segment that operates on diastolic phase. PPA behavior contextualized the situations where the hearts had been submitted, in respect to the Wext.
Análise proteômica de tecido cardíaco de ratos com diferente capacidade aeróbica intrínseca
(Universidade Federal do Espírito Santo, 2012-12-17) Ribeiro, Leonardo Perin; Lunz, Wellington; Figueiredo, Suely Gomes de; Mill, Jose Geraldo; Pires, Simone da Fonseca
Exercise capacity is a complex attribute that involves different physiological systems under the influence of both genetic and environmental factors. Related to genetic influence, results have shown that more than 70% of aerobic exercise capacity is intrinsically determined. In this work, a comparative proteomic approach, twodimensional gel electrophoresis (2D) combined with MALDI-TOF/TOF tandem mass spectrometry, was used to investigate possible molecular differences at the protein expression level between rats heart (left ventricle - LV) with distinct intrinsic exercise capacity. Low running performance (LRP) and high running performance (HRP) rats were categorized by a maximal exercise test protocol performed on a motor-driven treadmill, according to total distance performed (TDP). The running capacity of HRPs was 3.5 fold greater than LRPs. Protein expression profiling revealed 29 statistically significant (p<0,05) differences between HRP and LRP, and 15 of these proteins were identified by MALDI-TOF/TOF (MS and MS/MS). Robust alterations were detected in components involved in antioxidant and stress response, miofibrillar and cytoskeletal proteins. Contractile proteins were found to have special expression modification: α-myosin heavy chain-6, myosin light chain-1 and creatine kinase up regulation in LV of HRP rats on patterns in HCR. In contrast, LV of LRP rats exhibited increase in abundance of protein associated with stress response. These animals exhibited enhanced expression of the antioxidant enzyme (aldehyde dehydrogenase 2), and heat shock proteins (α-crystallin B chain, heat shock protein β-2). In addition, the cytoskeletal proteins, desmin and α-actin, were upregulated in LCRs. In conclusion, our results suggest that the increased contractile proteins levels in HCRs rats may explain, in part, the improved exercise capacity. The increased stress protein expression in LCR suggests that the LV proteome of these animals are exposed to greater stress
Análise temporal da função renal em camundongos hipercolesterolêmicos
(Universidade Federal do Espírito Santo, 2009-10-02) Balarini, Camille de Moura; Gava, Agata Lages; Meyrelles, Silvana dos Santos; Stefanon, Ivanita; Pereira, Thiago de Melo Costa
Aging is a physiological process with deleterious consequences for renal function, which could be exacerbated when concurrent with pathological situations, such as dyslipidemia. The aim of this study was to determine whether hypercholesterolemia and aging could affect the renal function in mice. Male hypercholesterolemic apolipoprotein E-deficient (ApoE, n=18) mice and their age-matched C57BL/6 (C57, n=18) control mice were studied at 2-, 4- and 8-month-old. At each time point, animals were placed in metabolic cages for 24 hours in order to analyze urine volume and urinary creatinine determination. Samples of blood were collected for serum cholesterol, urea and creatinine determination. Glomerular filtration rate (GFR) was estimated by the creatinine clearance. Urine samples were submitted to polyacrilamide gel electrophoresis to verify the presence of albuminuria and renal senescence was evaluated by senescence associated beta-galactosidase activity technique. Glomerular morphometric measurements were evaluated in 10 hematoxilin-eosin stained sections (10 µm-thickness) and mesangial expansion was evaluated by Periodic Acid Schiff staining. Expression of nNOS was measured by Western Blotting. For statistical analysis, 2-way ANOVA was used followed by Fisher’s post hoc. Differences were considered statistically significant when p<0.05. Total plasma cholesterol was increased about 5-fold in ApoE mice at both time points compared with C57 animals (C57 2 months: 94.0±5.1; ApoE 2 months: 606.0±91.3; C57 4 months: 97.1±7.2; ApoE 4 months: 493.7±44.0; C57 8 months: 116.0±10.0 and ApoE 8 months: 636.1±76.4). At 2-month-old, GFR was already markedly reduced in ApoE (187±28) when compared to C57 mice (358±92). Aging caused a significant reduction of GFR in C57 mice (4 months: 211±60 and 8 months: 81±14) although did not worse this parameter in ApoE mice (4 months: 128±42 and 8 months: 93±18). In addition, serum urea was significantly increased in ApoE animals already at 2-month-old compared with C57 mice and this difference is not time-dependent (C57 2 months: 39.8±5.2; ApoE 2 months: 64.5±7.6; C57 4 months: 41.1±7.8; ApoE 4 months: 73.5±17.9; C57 8 months: 49.1±3.5; ApoE 8 months: 77.3±7.5). Only ApoE mice at 8-montold presented albuminuria. Aging promoted markedly renal senescence in C57 animals and this occurred earlier in ApoE. No differences were found in glomeruli number nor glomerular tuft area. A significant mesangial expansion was already observed at 2-month-old ApoE mice (ApoE: 35.3±0.8 vs. C57: 29.8±0.9) and this condition was aggravated by aging in ApoE mice (4 months: 40.4±1.2 and 8 months: 41.5±2.7) and induced in age-matched C57 animals (4 months: 37.8±1.3 and 8 months: 37.4±0.7). No differences were found in nNOS expression due to neither aging nor hypercholesterolemia. These data show that hypercholesterolemia can enhance the age-related loss of renal function.
Análise temporal do número e genotoxicidade de células-tronco de medula óssea de camundongos ateroscleróticos
(Universidade Federal do Espírito Santo, 2008-08-04) Tonini, Clarissa Loureiro; Meyrelles, Silvana dos Santos; Arruda, Robéria Maria Mendes Pontes; Vasquez, Elisardo Corral; Mill, José Geraldo
Currently stem cells have been target of many studies, many of them using cellular therapy in the cardiovascular diseases. However, little is known about the mechanisms that modify function and mobilization of the stem cells when submitted to the senescence and atherosclerosis. The analysis of stem cells of the ApoE-KO mice disclosed that atherosclerosis increases the number of mesenchymal and hematopoietic cells on the bone marrow probably through the increase of the symmetrical divisions stimulated by the progression of the atherosclerotic plaque. Analysis of control group showed increased number of hematopoietic stem cells and diminished number of mesenchymal stem cells. Genotoxicity assay revealed high level of DNA fragmentation in the mononuclear cells of the bone marrow in the atherosclerotic group that occurs because of the production of free radicals in atherosclerosis, what also it was evidenced by the senescence of the analyzed aortic root. In contrast, the C57 group presented low level of DNA fragmentation and, therefore low vascular senescence. We also observed that aging increased the number of hematopoietic stem cell in this group, that is, this lineage of cells does not loss the proliferative capacity, and it does not happen with the mesenchymal lineage.
Angiotensina II intra-renal modula a expressão da óxido nítrico sintase neuronal na hipertensão renovascular 2R1C
(Universidade Federal do Espírito Santo, 2005-12-20) Pereira, Thiago de Melo Costa; Silva, Ian Victor; Meyrelles, Silvana dos Santos; Cabral, Antonio de Melo; Gouvêa, Sônia Alves; Soares, Luciana Saloto
In physiological conditions, nitric oxide (NO) exerts a modulatory influence on renal blood flow mainly due the neuronal nitric oxide synthase (nNOS) enzyme isoform. Although some studies have demonstrated that the renal nNOS mRNA expression is modified in arterial hypertension (HÁ), it has not yet been shown how nNOS protein expression is modulated by endogenous angiotensin II (Ang II), a vasoconstrictor and a NO function inhibitor. Through the western blotting technique have been evaluate the relative role of HA and Ang II on the nNOS protein expression in the kidneys of renovascular hypertensive rats two-kidneys one clip (2K1C). The specific aim was to investigate the role of AT1 receptors and oxidative stress in modulating nNOS expression and the NO bioavaiability by GMPc quantification for enzymeimmunoassay. Then, the animals were divided in 4 groups: 2K1C (n=9), 2K1C+subpressor dose of losartan (10 mg/Kg/day in drinking water; n=4), 2K1C+subpressor dose of tempol (0.2 mmol/Kg/day in drinking water; n=6), and Sham (n=16), presenting values of MAP 179 ± 5 mmHg, 140 ± 7 mmHg, 181 ± 10 mmHg and 99 ± 3 mmHg, respectively. The nNOS expression was increased in the contralateral and clipped kidneys of the animals 2R1C when compared to SHAM group (0,43±0,03 vs. 0,14 ± 0,02 u.d.o. e 0,27±0,03 vs. 0,16±0,03 u.d.o. respectively), normalized in both kidneys in 2R1C + losartan when compared to SHAM group (0,24 ± 0,01 vs 0,27 ± 0,01 u.d.o e 0,21 ± 0,03 vs.0,29 ± 0,02 u.d.o., respectively). In 2R1C + tempol group, the nNOS expression was decreased in the contralateral kidney (0,27 ± 0,06 vs. 0,19 ± 0,06 u.d.o., respectively) but still increased in the clipped kidney when compared to SHAM group (0,35 ± 0,08 vs. 0,17 ± 0,03 u.d.o., respectively). The present results demonstrate that: 1) In the 2K1C renovascular hypertension model, the AT1 receptors and oxidative stress seem to be primary stimuli for increasing nNOS expression but not the HA per se; 2) The increase in nNOS expression does not reflects directly on the more NO bioavaiability in both kidneys (contralaetral or clipped); 3) The increase in nNOS expression induces a compensatory mechanism in order to maintain the renal homeostasis in this model of hypertension.
Antagonista do receptor tipo AMPA reverte a modulação pré-frontal induzida pela estimulação epidural por corrente contínua na memória operacional espacial
(Universidade Federal do Espírito Santo, 2016-08-25) Martins, Cleciane Waldetário; Palacios, Ester Miyuki Nakamura; Rodrigues, Lívia Carla de Melo; Barauna, Valério Garrone; Valle, Ângela Cristina do
The modulation of the prefrontal cortex (PFC) excitability by direct current stimulation improves cognitive function. However, the underlying mechanisms remains unknown. Here we investigated the involvement of glutamate α-amino-3-hydroxy-5-methyl-4- isoxazole propionic acidreceptors (AMPARs) on the effects of repetitive epidural direct current stimulation (eDCS) on long-termed spatial working memory. Methods: Well-trained rats in 8-arm radial maze (8-RM) procedures received acute intraperitoneal (IP) administration of the AMPAR antagonist, perampanel (PRP, 1 mg/kg) or its vehicle (VEH) before performing 4-h delayed tasks in 8-RM. This drug intervention was performed before or after repetitive (once daily, five consecutive days) anodal eDCS (400 µA, 13 minutes) over the left medial PFC or sham procedure. Results: Animals treated with PRP (n = 27) showed larger number of errors (p < 0.01) in the 4-h post-delayed performance compared to those treated with VEH (n = 26). After the repetitive eDCS, animals treated with VEH (n = 13) presented smaller number of errors in the 4-h post-delay performance compared to animals receiving VEH after sham (p = 0.05, n = 12) and those receiving PRP after eDCS (p= 0.001, n = 13). These animals receiving PRP after eDCS showed larger (p = 0.025) number of errors when compared to those treated with PRP after sham (n = 12). Conclusions: AMPARs antagonism disrupted the spatial working memory and reversed the facilitating effects of the eDCS applied over the medial PFC. Thus, the spatial working memory and the prefrontal cognitive modulation by the direct current stimulation are highly dependent on AMPARs activity.

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