Controle hidroeletrolítico e respostas cardiovasculares à injeção central de angII, carbacol e hiperosmolaridade plasmática em ratos com epilepsia induzida por pilocarpina

• Autor(a) principal: Mercês, Thais Machado das
• Data de Publicação: 2019
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da UFG
• dARK ID: ark:/38995/0013000009cfh
• Texto Completo: http://repositorio.bc.ufg.br/tede/handle/tede/10305
• topic: Epilepsia do lobo temporal; Pilocarpina; Status epilepticus; Sistema renina angiotensina; Angiotensina II; Carbacol; Gavagem; Pressão arterial; Frequência cardíaca; Temporal lobe epilepsy; Pilocarpine; Status epilepticus; Renin system angiotensin; Angiotensin II; Carbachol; Gavage; Blood pressure; Heart rate; CIENCIAS BIOLOGICAS::FISIOLOGIA

Status epilepticus (SE) is a condition caused by failure of the mechanisms responsible for the termination of the seizure or the onset of the mechanism leading to abnormally prolonged seizures. An epileptic seizure is defined as “the transient occurrence of signs and/or secondary symptoms of abnormal brain neuronal activity”. Epilepsy is a brain syndrome defined by at least one of the following conditions: (1) less than 2 unprovoked epileptic seizures within 24 hours; (2) an unprovoked seizure in individuals who have factors associated with a higher likelihood of having a decreased epileptic threshold; (3) diagnosis of epilepsy syndrome. Individuals with epilepsy are more likely to suffer sudden death, with sudden and unexpected death in epilepsy (SUDEP) a more common category. The pilocarpine-induced epilepsy (PIE) model was the most used to study temporal lobe epilepsy (TLE). The renin angiotensin system (RAS) is known to be involved in some neurodegenerative diseases as well as epilepsy. And, it has been shown that the central nervous system (CNS) areas are responsible for thirst behavior and appetite for waste affected by the epilepsy model. Thus, this study aimed to study cardiovascular control in the face of changes in central levels of angiotensin II (Ang II), carbachol and plasma osmolarity in the PIE model. We used Wistar rats (250-280 g), preused with methylscopolamine (1mg / kg intraperitoneal -ip), after receiving a pilocarpine injection (350 mg / kg-ip) to induce SE. After 3 hours of SE, dizepam (10 mg / kg -i.p.) was injected to stop a seizure. Daily intake of water and 1,8% NaCl, no difference between groups, and body weight were made in which epilepsy group uses a lower weight gain when using a control group (358 ± 13 vs. 406 ± 6 g, respectively). Animals prepared with cannulae directed to the lateral ventricle (VL) were divided into two groups with which cardiovascular records were recorded: one group that removes intracerebroventricular (icv) injection from Ang II and the other one with carbachol. We observed that the pressor response was higher in the epilepsy group when compared to the control after Ang II injection (Epilepsy: 28,0 ± 3,3 vs. Control: 13,3 ± 0,7 mmHg, p <0,05). , a variation in heart rate (ΔHR) was not different between groups. In animals receiving icv carbacol injection, the response was not different between groups, but there was a difference between groups compared with baseline (-0,5 ± 1,4 vs. 22,3 ± 4,6 mmHg, epilepsy and 1,0 ± 2,3 vs. 24,3 ± 4,0 mmHg, control, p <0,05), ΔHR was different between groups (Epilepsy: -24,3 ± 6,1 vs. Control: - 56,3 ± 13,2 bpm), as well as within the control group, comparing their baseline period to the post-carbachol injection period (396,7 ± 17,0 vs. -56,3 ± 13,2 bpm, respectively). In another experiment, the animals were recorded after an intrinsic 12% NaCl overload, which showed a pressure drop at 30, 40 and 50 min in the epilepsy group when compared to 10 minutes after gavage ( 10 ': 5,6 ± 2,9 vs. 30': -8,0 ± 5,3 mmHg; 40 ': -11,5 ± 4,9 mmHg; 50': -9,0 ± 4,5 mmHg ). This was not observed in control animals. Regarding HR there was no difference between the groups, but no group with epilepsy increased after gavage when comparing the times -10, -1, 40, 50 and 60 minutes (10 ': 49,2 ± 23,0 vs. -10 ': 0,0 ± 0,0 bpm; -1': -5,7 ± 11,1 bpm; 40 ': 3,5 ± 7,3 bpm; 50': -7,0 ± 9,6 bpm and 60 ': -5,7 ± 11,3 bpm). Our results suggest that pilocarpine-induced epilepsy is capable of altering angiotensin, carbachol-dependent mechanisms and increased plasma osmolarity, which alter or control harmful blood pressure or corrective substance use and contribute to SUDEP.