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首页> 外文期刊>American Journal of Physiology >Effects of acute and chronic nitric oxide inhibition in an experimental model of chronic pulmonary allergic inflammation in guinea pigs.
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Effects of acute and chronic nitric oxide inhibition in an experimental model of chronic pulmonary allergic inflammation in guinea pigs.

机译：急性和慢性一氧化氮抑制作用在豚鼠慢性肺过敏性炎症实验模型中的作用。

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Endogenously produced nitric oxide is a recognized regulator of physiological lung events, such as a neurotransmitter and a proinflammatory mediator. We tested the differences between chronic and acute nitric oxide inhibition by N(omega)-nitro-L-arginine methyl ester (L-NAME) treatment in lung mechanics, inflammation, and airway remodeling in an experimental asthma model in guinea pigs. Both acute and chronic L-NAME treatment reduced exhaled nitric oxide in sensitized animals (P < 0.001). Chronic L-NAME treatment increased baseline and maximal responses after antigen challenge of respiratory system resistance and reduced peribronchial edema and mononuclear cells airway infiltration (P < 0.05). Acute administration of L-NAME increased maximal values of respiratory system elastance and reduced mononuclear cells and eosinophils in airway wall (P < 0.05). Chronic ovalbumin exposure resulted in airway wall thickening due to an increase in collagen content (P < 0.005). Chronic nitric oxide inhibition increased collagen deposition in airway wall in sensitized animals (P < 0.05). These data support the hypothesis that in this model nitric oxide acts as a bronchodilator, mainly in proximal airways. Furthermore, chronic nitric oxide inhibition was effective in reducing edema and mononuclear cells in airway wall. However, airway eosinophilic inflammation was unaltered by chronic L-NAME treatment. In addition, nitric oxide inhibition upregulates collagen deposition in airway walls.
机译：内源性产生的一氧化氮是公认的生理性肺事件的调节剂，例如神经递质和促炎介质。我们在豚鼠的实验性哮喘模型中测试了N（ω）-硝基-L-精氨酸甲酯（L-NAME）治疗对慢性和急性一氧化氮的抑制作用在肺力学，炎症和气道重塑中的差异。急性和慢性L-NAME治疗均可降低致敏动物的呼出气一氧化氮（P <0.001）。长期L-NAME治疗增加了对呼吸系统抵抗力的抗原攻击后的基线和最大反应，并降低了支气管周围水肿和单核细胞气道浸润（P <0.05）。急性给予L-NAME可增加呼吸系统弹性的最大值，并减少气道壁中的单核细胞和嗜酸性粒细胞（P <0.05）。由于胶原蛋白含量的增加，慢性卵白蛋白暴露导致气道壁增厚（P <0.005）。慢性一氧化氮抑制作用增加了致敏动物气道壁中胶原的沉积（P <0.05）。这些数据支持以下假设：一氧化氮主要在近端气道中充当支气管扩张剂。此外，慢性一氧化氮抑制可有效减少气道壁水肿和单核细胞。但是，慢性L-NAME治疗不会改变气道嗜酸性炎症。此外，一氧化氮抑制作用还可以上调胶原蛋白在气道壁中的沉积。

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