摘要
目的 观察吸入一氧化氮 (NO)对慢性和急性缺氧所致大鼠肺动脉高压的作用。 方法 分别利用雄性Wistar大鼠 3 0只 ,制备慢性和急性缺氧肺动脉高压模型。实验中监测肺动脉压、血气、高铁血红蛋白含量 (Met % )等指标。 结果 慢性缺氧大鼠吸入 2 0 ppm、40ppmNO ,肺动脉平均压 (MPAP)由治疗前 (2 5 2± 3 5 )mmHg降到 (2 2 4± 3 5 )mmHg及 (2 1 8± 3 3 )mmHg ,而对动物体循环血压无明显影响 ;急性缺氧大鼠吸入 2 0 ppm、40 ppmNO 1hMPAP分别由缺氧时 (2 2 8± 2 7)mmHg、(2 4± 2 8)mmHg下降到 (19 6± 4 7)mmHg和 (2 0 5± 4 1)mmHg。吸入NO 4h ,2 0ppm组Met %由 (0 40± 0 3 9) %升到 (0 95±0 75 ) % ,40 ppm组由 (0 3 9± 0 3 2 ) %升到 (1 2 6± 0 49) %。肺病理组织检查显示 :2 0 ppm、40 ppm组与对照组无显著差别。 结论 吸入NO对慢性和急性缺氧肺动脉高压具有选择性扩张肺血管的作用 ,急性缺氧大鼠持续吸入NO 4h不会引起高铁血红蛋白血症 。
Objective To study the effect of inhaled NO on pulmonary hypertension in rat models induced by chronic and acute hypoxia.Methods Thirty male wistar rats were involved for the chronic and acute hypoxic study respectively.Pulmonary artery pressure,blood gases and the level of methemoglobin(Met%) were measured during the experiments.Results In the models of chronic hypoxia,mean pulmonary artery pressure(MPAP) decreased from (25 2±3 5)mmHg to (22 4±3 5)mmHg and (21 8±3 3)mmHg respectively after inhaled 20 ppm and 40 ppm NO.Inhaled nitric oxide did not affect systemic arterial pressure.In the models of acute hypoxia,inhalation of 20 ppm and 40 ppm NO for 1 hour decreased MPAP from (22 8±2 7)mmHg and (24±2 8)mmHg to (19 6±4 7)mmHg and (20 5±4 1)mmHg respectively.There were significant increases in circulating methemoglobin from (0 40±0 39%) to (0 95±0 75%) at 20 ppm and from (0 39±0 32%) to (1 26±0 49%) at 40 ppm.But the increased methemoglobin values were still in normal range.In pathologic histologic study of lung,there were no significant differences among the control,20 ppm and 40 ppm NO inhaling groups.Conclusion The results suggested that inhaled NO may be a selective pulmonary vasodilator on chronic and hypoxic pulmonary hypertension.Treatment of inhaling 4 hours NO didn′t cause adverse effects.
出处
《小儿急救医学》
2001年第2期82-84,共3页
Pediatric Emergency Medicine
基金
北京市自然科学资金项目资助
