摘要
目的 研究内源性一氧化氮对低氧大鼠肺动脉血红素氧合酶 /一氧化碳体系的调节作用 ,以探讨一氧化氮对低氧性肺血管结构重建调节作用的机理。方法 将 2 1只大鼠随机分为 3组 :常氧组、低氧组和低氧 +L NAME组 (经NO合酶抑制剂Nω 硝基 L 精氨酸甲酯处理的低氧组 ) ,每组 7只。用免疫组织化学技术对肺动脉平滑肌细胞中血红素氧合酶 1的含量及定位进行分析 ,同时应用分光光度计检测 3组大鼠血浆和肺组织匀浆中一氧化碳含量。结果 低氧组大鼠肺动脉平滑肌细胞中血红素氧合酶 1表达与常氧组相比明显增强 (P <0 .0 1) ,而低氧 +L NAME组大鼠肺动脉平滑肌细胞中血红素氧合酶 1的表达又明显低于低氧组 (P <0 .0 1)。低氧组大鼠血浆和肺组织匀浆中一氧化碳含量明显高于常氧组 (P <0 .0 1) ,而低氧 +L NAME组大鼠血浆和肺组织匀浆中一氧化碳含量又明显低于低氧组 (P <0 .0 1)。结论 研究提示 ,内源性一氧化氮可通过内源性一氧化碳途径对低氧时肺循环进行调节。
Objective Endogenous nitric oxide (NO) could suppress hypoxic pulmonary vascular structural remodeling, but the exact mechanism is still unknown. Endogenous carbon monoxide (CO) is involved in the regulation of pulmonary circulation. However, whether heme oxygenase-1 (HO-1)/CO system is involved in the mechanisms by which NO regulates hypoxic pulmonary vascular structural remodeling is unclear. Therefore, the study aimed to explore the effect of endogenous NO on HO/CO system in pulmonary arteries of hypoxic rats by examining the effects of N ω-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase(NOS), on the expression of HO-1 in pulmonary artery smooth muscle cells of chronic hypoxic rats and the production of CO in plasma and pulmonary tissue homogenates. Methods Twenty-one Wistar rats were randomly divided into three groups: normoxia group ( n =7), hypoxia group ( n =7) and hypoxia +L-NAME group ( n =7). Hypoxic challenge was performed by putting the rats into a normobaric hypoxic chamber with an oxygen concentration of (10±0.5)% for two weeks, six hours per day. Every day before experiment L-NAME was administrated intraperitoneally at a dose of 5 mg/kg. The expressions of HO-1 in large, median and small pulmonary artery smooth muscle cells were observed under microscope. The indirect production of CO in plasma and pulmonary tissue homogenates was detected by the spectrophotometer. Results The results showed that the expressions of HO-1 by pulmonary artery smooth muscle cells of hypoxic rats significantly increased compared to that in normoxic group ( P <0.01). However, when L-NAME was used ,the expression of HO-1 in large and median pulmonary artery smooth muscle cells of hypoxic rats decreased significantly compared to that of hypoxic rats ( P <0.01). The HO-1 expression by small pulmonary artery smooth muscle cells of hypoxic rats also markedly increased ( P < 0.05). The plasma and pulmonary tissue homogenates CO concentrations in hypoxic rats significantly increased compared to that of normoxic rats ( P <0.01),while the level of CO decreased significantly when L-NAME was used ( P <0.01). Conclusion That endogenous nitric oxide might induce CO production in pulmonary arteries of hypoxic rats.
出处
《中华儿科杂志》
CAS
CSCD
北大核心
2000年第12期742-745,共4页
Chinese Journal of Pediatrics
基金
国家自然科学基金(39870844)
国家重点基础研究发展规划基金(G2000056905)
