Role of nitric oxide in hyperpnea-induced bronchoconstriction and airway microvascular permeability in guinea pigs

Author： Pennacchioni-Alves Patrííícia Vieira Rodolfo Paula Santos Lopes Fernanda Degobi Tenóóório Quirino Arantes-Costa Fernanda Magalhaes Pianheri Fabia B. Martins Milton Arruda Fernandes Carvalho Celso Ricardo

Publisher： Informa Healthcare

ISSN： 1521-0499

Source： Experimental Lung Research, Vol.36, Iss.2, 2010-03, pp. : 67-74

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Abstract

ABSTRACTThe 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, tracheotomized, 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-l-arginine methyl ester (l-NAME) (50 mg/kg), aminoguadinine (AG) (50 mg/kg), and l-arginine (100 mg/kg) and exhaled NO (NOex) was evaluated before and after drug administration and hyperpnea. The results show that l-NAME potentiated (57%%%) HIB and this effect was totally reversed by l-arginine pretreatment, whereas AG did not have effect on HIB. l-NAME decreased basal AMP (48%%%), but neither l-NAME nor AG had any effect on hyperpnea-induced AMP. NOex levels were decreased by 50%%% with l-NAME, effect that was reversed by l-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.