Liberação de angiotensina-(1-7) e alamandina no pós-condicionamento cardíaco isquêmico e farmacológico em coração isolado de ratos

• Ano de defesa: 2015
• Autor(a) principal: Renata da Cunha Ribeiro
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Pós-condicionamento isquêmico; Angiotensina-(1-7); Pós-condicionamento farmacológico; Pós-condicionamento cardíaco; Alamandina; Sistema renina angiotensina; Sevoflurano; Sistema renina-angiotensina Fisiologia; Angiotensina; Fisiologia
• Link de acesso: http://hdl.handle.net/1843/BUBD-9WHG9A

Background: Its know that ischemic lesions are often lethal to various organs such as heart, brain, lungs and intestines. Paradoxically, reperfusion may be as or more damaging than ischemia. In an attempt to minimize the damage caused by reperfusion different myocardial protection techniques have been studied in recent years. Conditioning techniques before ischemia (preconditioning) during ischemia (per-conditioning) and after ischemia (postconditioning) were tested by several authors with varying success rates. Some studies have demonstrated cardioprotective effect of angiotensin (1-7) in isolated hearts exposed to the phenomenon of ischemia / reperfusion. Objectives: The aim of this study is to clarify whether the renin angiotensin system, mainly through the angiotensin-(1-7), Angiotensin II and Alamandine, participates in the cardioprotection determined by cardiac post-conditioning methods (ischemic and pharmacological) in ischemic phenomenon / reperfusion in isolated hearts of male Sprague-Dawley rats. Materials and Methods: 18 male Sprague-Dawley rats, aged between 12 and 16 weeks were decapitated and their hearts were isolated and placed in the Langendorff apparatus where they were perfused with Krebs-Henseleit solution oxygenated with a mixture of 95% O2 / 5 % CO2. After being placed in the apparatus, was inserted through the left atrium one balloon positioned within the left ventricle in order to measure the physiological parameters. The ECG was recorded by placing electrodes on the heart surface. All parameters were recorded in real time by LabChart Pro® software. All groups were subjected to 30 min of stabilization followed by 30 minutes of infarction. The infarction was performed using the technique described by Lubbe et al (1). At the beginning of reperfusion, the animals were divided in three groups (n = 6):. In the control group was performed 60 minutes of reperfusion without interference. In ischemic postconditioning group at the beginning of reperfusion were performed three cycles of ischemia / reperfusion with 10s duration each. In the pharmacological postconditioning group inhalational anesthetic sevoflurane was connected to the oxygen circuit during the first 10 minutes of reperfusion 2.5% (CAM 1). In every heart there was periodic collection of perfusate to carry out the measurements of CK-MB, LDH, troponin I enzimes and angiotensin peptides angiotensin-(1-7), angioensin II and alamandine. Results: Several parameters varied in the opposite direction than expected and in most of them there was no significant difference between groups. We observed the same result with enzymes and peptides measured. Dosages of Alamandina and Angiotensin- (1-7) showed reduction as the reperfusion period compared to the period of ischemia in groups submitted to pharmacological postconditioning techniques. In the ischemic postconditioning group submitted was increased Alamandina for the period of ischemia, but it does not recovered the stabilization values. Angiotensin- (1-7) had a decrease when compared to the period of ischemia. Angiotensin II had a variable behavior, decreasing during reperfusion of the control group and pharmacological post-conditioning and increasing during reperfusion of ischemic post-conditioning group. Pharmacological post-conditioning group had the highest incidence of arrhythmias of the three groups. The control group had a lower incidence of arrhythmias in the whole period of reperfusion and ischemic post-conditioning group had a lower incidence in the first 5' de reperfusion. Conclusion: In our study, ischemia conducted was not sufficient to trigger the protection mechanisms observed in the post-conditioning and already described in other studies, but the angiotensin-(1-7) seem to decrease with post-conditioning techniques as alamandine and angiotensin II features a variable behavior. The angiotensin-(1-7) and alamandine suggest the antiarrhythmic effect.