| Texto completo | |
| Autor(es): |
Maia, Octavio A. C.
;
Malheiros-Lima, Milene R.
;
Oliveira, Maria A.
;
Castro, Claudio L.
;
Moriya, Henrique T.
;
Tavares-de-Lima, Wothan
;
Takakura, Ana C.
;
Moreira, Thiago S.
Número total de Autores: 8
|
| Tipo de documento: | Artigo Científico |
| Fonte: | Brain Research Bulletin; v. 161, p. 8-pg., 2020-08-01. |
| Resumo | |
One of the possible causes of death in epilepsy is breathing disorders, especially apneas, which lead to an increase in CO2 levels (hypercapnia) and/or a decrease in O-2 levels in arterial blood (hypoxemia). The respiratory neurons located in the ventral brainstem respiratory column are the main groups responsible for controlling breathing. Recent data from our group demonstrated respiratory changes in two experimental models of epilepsy, i.e. audiogenic epilepsy, and amygdala rapid kindling. Here, we aimed to evaluate respiratory changes in the classic model of temporal lobe epilepsy induced by intra-hippocampal injection of pilocarpine. Adult Wistar rats with stainless-steel cannulas implanted in the hippocampus region were used. The animals were submitted to pilocarpine injection (2.4 mg/mu L, N = 12-15) or saline (N = 9) into the hippocampus. The respiratory parameters analyzed by whole-body plethysmography were respiratory rate (f(R)), tidal volume (V-T) and ventilation (V-E). Respiratory mechanics such as Newtonian airway resistance (R-n), viscance of the pulmonary parenchyma (G) and the elastance of the pulmonary parenchyma (H) were also investigated. No changes in baseline breathing were detected 15 or 30 days after pilocarpine-induced status epilepticus (SE). However, 30 days after pilocarpine-induced SE, a significant reduction in V-E was observed during hypercapnic (7% CO2) stimulation, without affecting the hypoxia (8% O-2) ventilatory response. We also did not observe changes in respiratory mechanics. The present results suggest that the impairment of the hypercapnia ventilatory response in pilocarpine-induced SE could be related to a presumable degeneration of brainstem respiratory neurons but not to peripheral mechanisms. (AU) | |
| Processo FAPESP: | 16/23281-3 - Regiões encefálicas responsáveis pela neuroplasticidade observada na resposta respiratória induzida por hipercapnia em modelo animal de Doença de Parkinson |
| Beneficiário: | Ana Carolina Takakura Moreira |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |
| Processo FAPESP: | 15/23376-1 - Núcleo retrotrapezóide, quimiossensibilidade central e automaticidade respiratória |
| Beneficiário: | Thiago dos Santos Moreira |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |
| Processo FAPESP: | 17/08696-5 - Sinalização purinérgica na região do Núcleo Retrotrapezóide: contribuição para o controle respiratório no modelo de epilepsia do lobo temporal |
| Beneficiário: | Milene Rodrigues Malheiros Lima |
| Modalidade de apoio: | Bolsas no Brasil - Pós-Doutorado |