Efeitos da infusão contínua de Cetamina s(+) em equinos anestesiados pelo Halotano

The horse’s blood pressure is susceptible to changes induced by volatile anesthetics. Because of that, the use of anesthesic techniques which keep stable the horse´s blood pressure is essencial. Ketamine is an important induction and maintenance anesthetic agent used in the horse anesthesia practice mainly to improve the blood pressure. S(+)-ketamine provides the same effects on the blood pressure, with greater analgesic results and less side effects than the normal ketamine. Although some studies have been conducted with ketamine continuous rate infusion during the halothane anesthetized horses, the S(+)-ketamine has not been evaluated yet. Considering the increased use of ketamine, it is important to evaluate its cardiovascular and respiratory effects in halothane anesthetized horses. To conclude, S(+)-ketamine 0.01mg/kg/min. continuous rate infusion did not induce additive cardiovascular and respiratory depression in halothane anesthetized horses.

Polimorfismos genéticos como moduladores do consumo alimentar, peso corporal e comorbidades após um ano de cirurgia bariátrica

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Sintomas nasais, parâmetros hemodinâmicos e perfil inflamatório nasal e sistêmico de cortadores de cana-de-açúcar expostos à queima de biomassa

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Avaliação do desempenho de dois monitores oscilométricos portáteis na estimativa da pressão arterial direta em gatos anestesiados com isofluorano

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Comparação entre índices dinâmicos e volumétricos de pré-carga em cães submetidos à hemorragia moderada seguida de reposição volêmica

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Influência da suplementação de açaí (Euterpe oleracea Mart.) na ração sobre remodelação cardíaca em ratos expostos à fumaça do cigarro

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Efficiency and costless of a long-term physical exercise program to nom-medicated hypertensive males

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Effect of gestational protein restriction on left ventricle hypertrophy and heart angiotensin II signaling pathway in adult offspring rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Efeitos da exposição ao pesticida fipronil nas alterações pressóricas em ratos acordados

Pós-graduação em Ciências Biológicas (Farmacologia) - IBB

Impacto do exercício físico combinado na função diastólica de pacientes com insuficiência cardíaca e fração de ejeção reduzida

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Aplicação pré-operatória imediata de antimicrobianos e repercussão cardiorrespiratória e hemodinâmica em cadelas e gatas anestesiadas com isoflurano

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Non-invasive brain stimulation for the management of arterial hypertension

The neural control of the cardiovascular system is a complex process that involves many structures at different levels of nervous system. Several cortical areas are involved in the control of systemic blood pressure, such as the sensorimotor cortex, the medial prefrontal cortex and the insular cortex. Non-invasive brain stimulation techniques - repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) - induce sustained and prolonged functional changes of the human cerebral cortex. rTMS and tDCS has led to positive results in the treatment of some neurological and psychiatric disorders. Because experiments in animals show that cortical modulation can be an effective method to regulate the cardiovascular system, non-invasive brain stimulation might be a novel tool in the therapeutics of human arterial hypertension. We here review the experimental evidence that non-invasive brain stimulation can influence the autonomic nervous system and discuss the hypothesis that focal modulation of cortical excitability by rTMS or tDCS can influence sympathetic outflow and, eventually, blood pressure, thus providing a novel therapeutic tool for human arterial hypertension. (C) 2009 Published by Elsevier Ltd.

Resting heart rate as a predictor of metabolic dysfunctions in obese children and adolescents

Background: Recent studies have identified that a higher resting heart rate (RHR) is associated with elevated blood pressure, independent of body fatness, age and ethnicity. However, it is still unclear whether RHR can also be applied as a screening for other risk factors, such as hyperglycemia and dyslipidemia. Thus, the purpose of the presented study was to analyze the association between RHR, lipid profile and fasting glucose in obese children and adolescents. Methods: The sample was composed of 180 obese children and adolescents, aged between 7-16 years. Whole-body and segmental body composition were estimated by Dual-energy X-ray absorptiometry. Resting heart rate (RHR) was measured by heart rate monitors. The fasting blood samples were analyzed for serum triglycerides, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and glucose, using the colorimetric method. Results: Fasting glucose, TC, triglycerides, HDL-C, LDL-C and RHR were similar in both genders. The group of obese subjects with a higher RHR presented, at a lower age, higher triglycerides and TC. There was a significant relationship between RHR, triglycerides and TC. In the multivariate model, triglycerides and TC maintained a significant relationship with RHR independent of age, gender, general and trunk adiposity. The ROC curve indicated that RHR has a high potential for screening elevated total cholesterol and triglycerides as well as dyslipidemia. Conclusion: Elevated RHR has the potential to identify subjects at an increased risk of atherosclerosis development.

A study of effectiveness of midazolam sedation for prevention of myocardial arrhythmias in endosseous implant placement

Purpose: The study aimed to assess electrocardiographic alterations during oral implant placement surgeries under local anesthesia (lidocaine chlorhydrate with epinephrine), using 15 mg of midazolam as an anxiolytic premedication. Material and methods: The study randomly selected 20 patients, aged 21-50 years old, requiring bilateral mandibular dental implants. Each patient was assessed using placebo on one side and midazolam on the contralateral side, with random, double-blinded distribution. The electrocardiogram recorded 12 static leads every 2 min, while D2 derivations were recorded continuously. Results: No statistically significant differences were observed between the placebo and midazolam when analyzing the morphological behavior of the electrocardiographic wave and the presence of arrhythmias during the experiment. However, under sedation, assessment of the behavior of electrocardiographic parameters during different stages of the procedure revealed statistically significant differences (P<0.05) for heart rate, P-wave amplitude and duration of the RR and QTc intervals. The arrhythmias detected were considered low risk for patients without systemic alterations and were observed in 53.3% of patients. The most frequently occurring alterations were tachycardia, bradycardia, supraventricular and ventricular extrasystoles and blocked atrial extrasystole, which were similar for both placebo and midazolam, with the greatest incidence during the initial, incision and bone drilling stages. Conclusion: The use of 15 mg of midazolam made no difference compared with the placebo. The use of 15 mg of midazolam did not show an advantage in the incidence of arrhythmias The anxiolytic premedication does not prevent myocardial arrhythmias in endosseous implant placement. The clinical significance of the arrhythmias may not represent serious risks.

beta-ADRENOCEPTORS IN THE MEDIAL AMYGDALOID NUCLEUS MODULATE THE TACHYCARDIAC RESPONSE TO RESTRAINT STRESS IN RATS

In the present study, we investigated the involvement of beta-adrenoceptors in the medial amygdaloid nucleus (MeA) in cardiovascular responses evoked in rats submitted to an acute restraint stress. We first pretreated Wistar rats with the nonselective beta-adrenoceptor antagonist propranolol microinjected bilaterally into the MeA (10, 15, and 20 nmol/100 nL) 10 min before exposure to acute restraint. The pretreatment with propranolol did not affect the blood pressure (BP) increase evoked by restraint. However, it increased the tachycardiac response caused by acute restraint when animals were pretreated with a dose of 15 nmol, without a significant effect on the BP response. This result indicates that beta-adrenoceptors in the MeA have an inhibitory influence on restraint-evoked heart rate (HR) changes. Pretreatment with the selective beta(2)-adrenoceptor antagonist ICI 118,551 (10, 15, and 20 nmol/100 nL) significantly increased the restraint-evoked tachycardiac response after doses of 15 and 20 nmol, an effect that was similar to that observed after the pretreatment with propranolol at a dose of 15 nmol, without a significant effect on the BP response. Pretreatment of the MeA with the selective beta(1)-adrenoceptor antagonist CGP 20712 (10, 15, and 20 nmol/100 nL) caused an opposite effect on the HR response, and a significant decrease in the restraint-evoked tachycardia was observed only after the dose of 20 nmol, without a significant effect on the BP response. Because propranolol is an equipotent antagonist of both beta(1) and beta(2)-adrenoceptors, and opposite effects were observed after the treatment with the higher doses of the selective antagonists ICI 118,551 and CGP 20712, the narrow window in the dose-response to propranolol could be explained by a functional antagonism resulting from the simultaneous inhibition of beta(1) and beta(2)-adrenoceptors by the treatment with propranolol. The present results suggest that beta(2)-adrenoceptors have an inhibitory influence on the restraint-evoked tachycardiac response, whereas beta(1)-adrenoceptors have a facilitatory influence on the restraint-evoked tachycardiac response. (c) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.