吸入一氧化碳对急性缺氧性肺动脉高压及缺氧性肺损伤的影响  

Effects of carbon monoxide inhalation on acute hypoxic pulmonary arterial hypertension and acute hypoxic lung injury J

作　　者：丁学琴[1] 刘贵明[1] 王俊科[1] 盛卓人[1] 孙新艳[1] 

机构地区：[1]中国医科大学第一附属医院麻醉科,沈阳110001

出　　处：《中华麻醉学杂志》2003年第5期361-364,共4页Chinese Journal of Anesthesiology

摘　　要：目的 研究吸入一氧化碳(CO)对急性缺氧性肺动脉高压及缺氧性肺损伤的影响。方法 30只大鼠随机分为三组:对照组(n=10):吸入21％0:30 min;缺氧组(n=10):吸入10％O2与90％N2的缺氧混合气30 min;CO组(n:10):吸入100 ppm CO与10％O2+90％N2的混合气30 min。随后取动脉血进行血气分析及碳氧血红蛋白测定,并测定血浆丙二醛(MDA)浓度及红细胞超氧化物歧化酶(SOD)的活性,放血处死大鼠后,速取右肺肺组织样本,戊二醛磷酸缓冲液固定后,采用透射电镜检查肺超微结构的变化。结果 与对照组比较,缺氧组平均肺动脉压(MPAP)明显升高,MDA水平增加,SOD活性降低,肺超微结构发生了病理改变;与缺氧组比较,CO组MPAP明显下降,PaO2明显增加,MDA水平下降,SOD活性升高,肺超微结构明显改善。结论吸入CO可改善缺氧大鼠的氧合,降低肺动脉压,减少氧自由基产生,从而减轻了急性肺损伤。Objective To investigate the effect of carbon monoxide (CO) inhalation on acute hypoxic pulmonary arterial hypertension and acute hypoxic lung injury. Methods Thirty Wistar rats weighing 180-250 g were anesthetized with intramuscular 3% pentobarbital 50 mg·kg-1 . Pulmonary catheter was inserted via right external jugular vein for mean pulmonary arterial pressure (MPAP) monitoring. Left common carotid artery was cannulated for BP monitoring. Tracheotomy was performed and the animals were mechanically ventilated ( RR = 80-90 bpm). PETCO2 was maintained at 35-45 mm Hg. The animals were randomly divided into 3 groups: (1) control group inhaled 21 % O2 for 30 min ( n = 10); (2) hypoxia group inhaled 10% O2 + 90% N2 for 30 min ( n = 10) and (3) CO group inhaled 100 ppm CO in 10% O2 + 90% N2 for 30 min ( n = 10) . Arterial blood 4 ml was obtained at the end of experiment for estimation of blood HbCO and plasma MDA concentration and RBC SOD activity. A piece of lung tissue was obtained immediately after the animal was sacrificed for electron microscopic examination. Results (1) In hypoxia group MPAP was markedly increased, plasma MDA level elevated and SOD activity reduced as compared with control group ( P < 0.01 ), and ultrastructural pathological changes were observed. (2) In CO group, MPAP was markedly decreased, PaO, was significantly increased as compared with hypoxia group, and there were significantly less ultrastructural pathological changes. Conclusion Inhalation of CO can improve oxygenation as shown by increased PaO2 , decrease hypoxia-induced high MPAP and oxygen free radicals and ameliorate acute lung injury.

关 键 词：急性缺氧性肺动脉高压 缺氧性肺损伤 一氧化碳 丙二醛 超氧化物歧化酶 碳氧血红蛋白 

分 类 号：R614[医药卫生—麻醉学]