| Registro completo |
| Provedor de dados: |
BJMBR
|
| País: |
Brazil
|
| Título: |
Role of nitric oxide in hypoxia-induced hyperventilation and hypothermia: participation of the locus coeruleus
|
| Autores: |
Fabris,G.
Anselmo-Franci,J.A.
Branco,L.G.S.
|
| Data: |
1999-11-01
|
| Ano: |
1999
|
| Palavras-chave: |
Nitric oxide
Locus coeruleus
Hypoxia
Ventilation
Body temperature
Rat
|
| Resumo: |
Hypoxia elicits hyperventilation and hypothermia, but the mechanisms involved are not well understood. The nitric oxide (NO) pathway is involved in hypoxia-induced hypothermia and hyperventilation, and works as a neuromodulator in the central nervous system, including the locus coeruleus (LC), which is a noradrenergic nucleus in the pons. The LC plays a role in a number of stress-induced responses, but its participation in the control of breathing and thermoregulation is unclear. Thus, in the present study, we tested the hypothesis that LC plays a role in the hypoxia-induced hypothermia and hyperventilation, and that NO is involved in these responses. Electrolytic lesions were performed bilaterally within the LC in awake unrestrained adult male Wistar rats weighing 250-350 g. Body temperature and pulmonary ventilation (VE) were measured. The rats were divided into 3 groups: control (N = 16), sham operated (N = 7) and LC lesioned (N = 19), and each group received a saline or an NG-nitro-L-arginine methyl ester (L-NAME, 250 µg/µl) intracerebroventricular (icv) injection. No significant difference was observed between control and sham-operated rats. Hypoxia (7% inspired O2) caused hyperventilation and hypothermia in both control (from 541.62 ± 35.02 to 1816.18 ± 170.7 and 36.3 ± 0.12 to 34.4 ± 0.09, respectively) and LC-lesioned rats (LCLR) (from 694.65 ± 63.17 to 2670.29 ± 471.33 and 36 ± 0.12 to 35.3 ± 0.12, respectively), but the increase in VE was higher (P<0.05) and hypothermia was reduced (P<0.05) in LCLR. L-NAME caused no significant change in VE or in body temperature under normoxia, but abolished both the hypoxia-induced hyperventilation and hypothermia. Hypoxia-induced hyperventilation was reduced in LCLR treated with L-NAME. L-NAME also abolished the hypoxia-induced hypothermia in LCLR. The present data indicate that hypoxia-induced hyperventilation and hypothermia may be related to the LC, and that NO is involved in these responses.
|
| Tipo: |
Info:eu-repo/semantics/article
|
| Idioma: |
Inglês
|
| Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1999001100009
|
| Editor: |
Associação Brasileira de Divulgação Científica
|
| Relação: |
10.1590/S0100-879X1999001100009
|
| Formato: |
text/html
|
| Fonte: |
Brazilian Journal of Medical and Biological Research v.32 n.11 1999
|
| Direitos: |
info:eu-repo/semantics/openAccess
|
|
