Pennacchioni-Alves Patrícia, Vieira Rodolfo Paula, Santos Lopes Fernanda Degobi Tenório Quirino, Arantes-Costa Fernanda Magalhaes, Pianheri Fabia B, Martins Milton Arruda, Fernandes Carvalho Celso Ricardo
Department of Physical Therapy, University of Sao Paulo, Sao Paulo, Brazil.
Exp Lung Res. 2010 Mar;36(2):67-74. doi: 10.3109/01902140903103464.
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, 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.
本研究旨在评估一氧化氮（NO）在通气过度诱发的支气管收缩（HIB）及气道微血管通透性增高（AMP）中的作用。64只豚鼠麻醉后行气管切开、插管，并连接动物呼吸机以获取肺脏基线呼吸系统阻力（Rrs）。随后让动物进行5分钟的通气过度，并在通气过度后的15分钟内评估Rrs。通过气道组织中伊文思蓝染料（25mg/kg）外渗来评估AMP。通过用N（G）-硝基-L-精氨酸甲酯（L-NAME）（50mg/kg）、氨基胍（AG）（50mg/kg）和L-精氨酸（100mg/kg）预处理动物来评估组成型和诱导型NO，并在给药及通气过度前后评估呼出NO（NOex）。结果显示，L-NAME增强了（57%）HIB，且L-精氨酸预处理可完全逆转这一效应，而AG对HIB无作用。L-NAME降低了基础AMP（48%），但L-NAME和AG对通气过度诱发的AMP均无任何作用。L-NAME使NOex水平降低了50%，L-精氨酸治疗可逆转这一效应。这些结果表明，组成型而非诱导型NO可能对豚鼠的HIB具有支气管保护作用。作者还观察到，组成型和诱导型NO似乎对通气过度诱发的AMP均无任何作用。
