Avaliação reatividade aórtica, função ventricular e suscetibilidade a arritmias cardíacas de ratos submetidos ao modelo de indução de epilepsia pela pilocarpina

Abstract

The mechanism of sudden death in epilepsy (SUDEP) is not yet elucidated. Cardiac function impairment is identified as the likely mechanism. Our objective was to evaluate the cardiovascular function of rats submitted to the pilocarpine model of epilepsy. Materials and Methods: Wistar rats weighing 250 g at the beginning of the experiments were randomly divided into two equal groups: The Epilepsy group in which animals were subjected to an injection of pilocarpine (350mg / kg ip) preceded (30 minutes) by Methyl scopolamine (1 mg / kg ip) and status epilepticus was blocked after three hours with diazepam (10 mg / kg ip). Video monitoring (24hs/day) was performed. The control rats went through exactly the same procedure, but did not develop spontaneous seizures or status epilepticus. Rats at one month of epilepsy were sacrificed and had heart and thoracic aorta dissected. Constant Pressure modified langendorff was performed to evaluate ventricular function and arrhythmias tests induced by the protocol of ischemia / reperfusion. For evaluation of the aortic rings reactivity, curves of phenylephrine and acetylcholine (10-10 - 10-6 mol / L) were performed. At the end of the experiments the hearts were prepared for histological analysis (picrossírius) and also molecular biology (Kir 6.1 and Kir 6.2). Results: showed that the hearts of rats with epilepsy had worsened ventricular function during ischemia compared with the control group, but before and after ischemia did not find significant differences. The aortic rings of rats with epilepsy are less responsive to phenylephrine than control rats. Regarding the histological and molecular biological analyses, our results showed that the hearts of rats with epilepsy have higher collagen deposition than control groups. Conclusion: Our results point to significant worsening of cardiac tissue and the ventricular function at ischemia, which may contribute to SUDEP.