Tan Xun, Hu Song-Hua, Wang Xiao-Long
Department of Veterinary Medicine, Zhejiang University, Hangzhou, PR China.
Avian Pathol. 2007 Aug;36(4):261-7. doi: 10.1080/03079450701460765.
Nitric oxide (NO) produced by vascular endothelial cells is an important determinant of the basal tone of small arteries and arterioles. Impaired endothelial NO production has been implicated in the pathophysiology of pulmonary hypertension in humans. Available data suggest that reduction of endothelial NO synthesis, with evidence of reduced endothelial NO synthase expression in pulmonary arterioles, is associated with increased pulmonary vasomotor tone and vascular remodelling in hypertensive broilers. Supplemental l-arginine, a precursor of NO, has been shown to induce flow-dependent pulmonary vasodilation, to prevent reduced endothelial NO synthase expression and to inhibit vascular remodelling in broilers with pulmonary hypertension. Nevertheless, its effect on pulmonary hypertension syndrome incidence is limited. It appears that impaired production of NO is a secondary rather than a causative factor in the pathogenesis of pulmonary hypertension in broilers.
血管内皮细胞产生的一氧化氮（NO）是小动脉和微动脉基础张力的重要决定因素。内皮一氧化氮生成受损与人类肺动脉高压的病理生理学有关。现有数据表明，肺动脉小动脉中内皮一氧化氮合酶表达降低，内皮一氧化氮合成减少，这与高血压肉鸡肺血管运动张力增加和血管重塑有关。补充NO的前体L-精氨酸已被证明可诱导流量依赖性肺血管舒张，防止内皮一氧化氮合酶表达降低，并抑制患有肺动脉高压的肉鸡的血管重塑。然而，其对肺动脉高压综合征发病率的影响有限。看来，NO生成受损在肉鸡肺动脉高压发病机制中是一个次要而非致病因素。
