一氧化氮对缺氧性肺动脉高压大鼠血流动力学及肺组织结构的影响

Effeets of Inhaled Nitric Oxide on Hemodyamics and Lung Ultrastructure in Chronic Hypoxic Pulmonary Hypertensive Rats

为探讨吸入一氧化氮（NO）对慢性缺氧性肺动脉高压的疗效及毒副作用，本文对正常（NN）组和慢性缺氧（HN）组大鼠吸入10～80ppmNO测定其血流动力学、血气和高铁血红蛋白（MetHb）变化，并对正常对照（NC）组、慢性缺氧对照（HC）组、NN组和HN组肺组织进行常规组织学及透射电镜观察。结果显示：HN组吸入NO后，肺动脉平均压（mPAP）和肺血管阻力（PVR）明显降低，且PVR降低程度与NO浓度呈效量依赖性，但吸人80PPmN时mPAP未较吸入40ppmNO时进一步降低；吸入NO对NN组和HN组体循环血流动力学、血气、MetHb含量及NN组mPAP和PVR均无明显影响；HE染色光镜和透射电镜显示HC和HN组肺的组织学及超微结构均呈慢性缺氧改变，但未发现NN组较NC组、HN组较HC组之肺组织学和超微结构有明显恶化改变。提示短时吸入低浓度NO对降肺动脉高压具有选择性、安全及无毒副作用等特点。

To investigate whether hitric oxide (NO) might mwhate Pulmonary vasodilation in chronic hypoxic pulmonary hypertersive (CHPH) rats, we examined the effects of inhaled 10-80 ppm(gh per million) NO on the hemodynamics, blood gas plasma methernoglobin (MetHb) level, and lung histology as well as ultrastructure in rats. In CHPH rats, inhalation of NO sighficantly decreased mean pulmonary arterial pressure (mPAP) and pulmonary resistance (PVR) (P<0. 01). There was a dose-dependant relationship between fall Of PVR and Noconcettration.Howeveer, the lowering of mPAP caused by inhaling 80PPm NO is not sighficantly different fromthat by inhaling 40ppm NO. Few effects on systemic hemodynamics, blood gas, and Plasma MetHb level were ob diServed in both CHPH and normal rats. Moreover, no change Of mPAP and PVR was detected in normal rats. observation of HE stain and electron mioroscopy showed that there was a chronic hypoxic change in histology and ultrastructure of the lungs of chronic hypoxic control rats and CHPH rats with an inhalation of NO, but no further deterioration of morphological change was detected in these animals. In addition, normal control rats and normal rats with an irhaation of NO shawed a norrmal histologic and ultrastructural appe of lung. It is suggested that reducticon of pulmonary arterial hypertension by shart term inhalation of low dose NO was characterized by selectivity,safety, and few toxic and side effects.