血管紧张素转换酶抑制剂对化学性急性呼吸窘迫综合征治疗作用的实验研究

目的　探讨血管紧张素转换酶抑制剂 (ACEI)在急性呼吸窘迫综合征 (ARDS)治疗中的具体作用。方法　将大鼠分为对照组、ARDS组和卡托普利 (Cap)组 ,后 2个组按不同取血时间再分为6个亚组 ,每组大鼠 5～ 6只。观察投用ACEI类药物Cap对油酸所致ARDS大鼠生理、生化指标及循环内皮细胞 (CEC)的影响。结果　在全身血压保持在正常水平下 ,Cap对ARDS有一定疗效。 2h时ARDS大鼠肺动脉压从 (2 3 5 0± 5 79)mmHg(1mmHg =0 133kPa)降到接近正常的 (14 4 3± 1 5 1)mmHg;反映肺毛细血管内皮损伤情况的CEC数量从 (6 88± 1 90 ) / 0 9μl减少到 (4 2 5± 0 2 0 ) /0 9μl;动脉血氧分压从 (35 0 8± 4 5 9)mmHg上升到 (70 4 8± 9 5 4 )mmHg ,同时肺湿干重等指标已接近正常 ;说明即使投用大剂量油酸亦仅能引起轻度肺损伤。结论　ACEI能降低肺动脉高压 ,阻抑ARDS的病情进展并对肺血管内皮细胞有一定保护作用

An experimental study of therapeutic effect of ACEI on chemical-induced ARDS in rats

OBJECTIVE: To investigate the role of angiotensin converting enzyme inhibitor (ACEI) in the treatment of acute respiratory distress syndrome (ARDS). METHODS: Changes in physiological and biochemical indexes, and circulating endothelial cells (CEC) were observed in rats of oleic acid-induced ARDS with ACEI-Captopril (Cap) therapy and controls, respectively. RESULTS: Under the normal systemic blood pressure, Captopril therapy showed good effect on ARDS in rats. Two hours after administration of Captopril, their pulmonary arterial pressure reduced to (14.43 +/- 1.51) mm Hg (1 mm Hg = 0.133 kPa), approximating to normal level, from (23.50 +/- 5.79) mm Hg. The number of CEC, which reflected injuries in pulmonary capillaries, decreased to (4.25 +/- 0.20)/0.9 micro l from (6.88 +/- 1.90)/0.9 micro l. Value of oxygen pressure in arterial blood (PaO(2)) increased to (70.48 +/- 9.54) mm Hg from (35.08 +/- 4.59) mm Hg. In the mean time, ratio of wet to dry lung weight was returned to nearly normal. So, it indicated that high-dose of oleic acid could only induce mild lung injury, and the development of ARDS was obviously inhibited by ACEI. CONCLUSIONS: ACEI may effectively depress pulmonary arterial hypertension, block the development of ARDS, and have certain good protective effect on pulmonary capillary endothelia.