一氧化氮介导大鼠低氧性肺动脉高压的实验研究

Experimental Study of Hypoxic Pulmonary Hypertension Induced by Nitric Oxide in Rats

为了解一氧化氮（ＮＯ）在低氧性肺动脉高压中的作用，并探讨其可能机理，检测正常对照组及缺氧１、２、３周组大鼠血浆ＮＯ水平，并给缺氧２周组大鼠注入左旋精氨酸及ＮＧ－硝基－左旋精氨酸，观察其对大鼠血流动力学及肺病理改变的影响。结果：ＮＯ水平在缺氧１、２、３周时分别为５±２．６７μｍｏｌ／Ｌ、２．１±０．４１μｍｏｌ／Ｌ和０．５±０．１６μｍｏｌ／Ｌ，明显低于正常对照组６．７３±１．８３μｍｏｌ／Ｌ（Ｐ＜０．０５）。缺氧２周组注入左旋精氨酸（１００ｍｇ／ｋｇ）后可减轻肺动脉高压，但联合左旋精氨酸＋ＮＧ－硝基左旋精氨酸则不能使之减轻。病理检查显示缺氧２周组大鼠肺小动脉管壁增厚、管腔狭窄，左旋精氨酸可减轻该现象，而ＮＧ－硝基－左旋精氨酸则使之加重。上述实验结果表明，缺氧可使ＮＯ合成减少，升高肺动脉压；左旋精氨酸能减轻低氧性肺动脉高压，而ＮＧ－硝基－左旋精氨酸则拮抗其作用。

This experiment in rats was designed to investigate the effect and mechanism of nitric oxide (NO) in the induction of hypoxic pulmonary hypertension. The plasma concentrations of NO in normal controls and in the 1 , 2 and 3 week hyporemic ventilation groups were measured. The hemodynamic and pathological changes were observed in rats of the 2 week group after bolus injection of L Arginine and NG nitro L arginine. The results showed that NO concentrations of the 1 2 and 3 week groups were 5±2.67μmol/L 2.1±0.41μmol/L and 0.5±0.16μmol/L respectively, which were significantly lower than the control group′s 6.73±1.83μmol/L( P <0.05). Bolus injection of L Arginine 100mg·kg -1 ·d -1 could relieve chronic hypoxic pulmonary hypertension and decrease the thickening of pulmonary arteries, but L NNA could antagonize the effect of L Arginine. This experiment demonstrates that chronic hypoxemia may decrease the release of NO and result in pulmonary hypertension. L Arginine may be used to relieve pulmonary hypertension, but L NNA may antagonize the effect of L Arginine.