Artículos de revistas
Role of nitric oxide in hyperpnea-induced bronchoconstriction and airway microvascular permeability in guinea pigs
Fecha
2010Registro en:
EXPERIMENTAL LUNG RESEARCH, v.36, n.2, p.67-74, 2010
0190-2148
10.3109/01902140903103464
Autor
PENNACCHIONI-ALVES, Patricia
VIEIRA, Rodolfo Paula
LOPES, Fernanda Degobi Tenorio Quirino Santos
ARANTES-COSTA, Fernanda Magalhaes
PIANHERI, Fabia B.
MARTINS, Milton Arruda
CARVALHO, Celso Ricardo Fernandes
Institución
Resumen
The present study aimed to evaluate the role of nitric oxide (NO) on hyperpnea-induced bronchoconstriction (HIB) and airway microvascular hyperpermeability (AMP). Sixty-four guinea pigs were anesthetized, tracheotonnized, cannulated, and connected to animal ventilator to obtain pulmonary baseline respiratory system resistance (Rrs). Animals were then submitted to 5 minutes hyperpnea and Rrs was evaluated during 15 minutes after hyperpnea. AMP was evaluated by Evans blue dye (25 mg/kg) extravasation in airway tissues. Constitutive and inductible NO was evaluated by pretreating animals with N(G)-nitro-1-arginine methyl ester (I-NAME) (50 mg/kg), aminoguadinine (AG) (50 mg/kg), and I-arginine (100 mg/kg) and exhaled NO (NOex) was evaluated before and after drug administration and hyperpnea. The results show that I-NAME potentiated (57%) HIB and this effect was totally reversed by I-arginine pretreatment, whereas AG did not have effect on HIB. I-NAME decreased basal AMP (48%), but neither I-NAME nor AG had any effect on hyperpnea-induced AMP. NOex levels were decreased by 50% with I-NAME, effect that was reversed by I-arginine treatment. These results suggest that constitutive but not inducible NO could have a bronchoprotective effect on HIB in guinea pigs. The authors also observed that neither constitutive nor inducible NO seems to have any effect on hyperpnea-induced AMP.