卡托普利后处理对再灌注损伤鼠肺血管紧张

目的探讨卡托普利后处理对大鼠肺缺血—再灌注时肺血管内皮血管紧张素转换酶(ACE)mRNA表达的影响,分析其可能的作用机制。方法实验大鼠24只,随机分为假手术组(Sham组,n=8只)、缺血—再灌注组(I/R组,n=8只)和卡托普利后处理组(CAP组,n=8只)。I/R组阻断左肺门1 h后,恢复通气再灌注1 h。Sham组开胸游离左肺门,通气及灌注2 h。CAP组于再灌注前20 min腹腔注射卡托普利(10 mg.kg-1)行药物后处理,恢复通气再灌注1 h。留取静脉血及左侧肺组织,分别测定肺组织中髓过氧化物酶(MPO)、丙二醛(MDA)、超氧化物歧化酶(SOD)含量、ACE mRNA的表达量及静脉血中ET-1的含量,测肺湿/干重比(W/D)及光镜下观察肺组织病理变化。结果 CAP组肺组织MPO、MDA的含量及ACE mRNA的表达量、血清ET-1含量及肺W/D明显低于I/R组(P0.05);CAP组肺组织中SOD含量明显高于I/R组(P0.05);CAP组肺组织形态学损伤较I/R组明显减轻。结论卡托普利后处理可以明显减轻鼠肺缺血再灌注损伤,其机制可能与其抑制缺血再灌注损伤鼠肺组织中ACE mRNA的表达有关。

Effects of captopril postconditioning on mRNA expression of angiotensinconvertion enzyme in lung ischemia-reperfusion injury in rats

Objective To investigate the effects of captopril postconditioning on mRNA expression of angiotensin-convertion enzyme （ACE） in pulmonary vascular endothelium during lung ischemia-reperfusion injury in rats and to analyze its possible mechanisms. Meth- ods Twenty-four rats were randomly assigned into three groups ： a Sham operation group （ Sham group, n = 8 ）, an ischemia-reperfusion group （ I/R group, n = 8 ） and a captopril postconditioning group （ CAP group, n = 8 ）. As for Sham group, left thoracotomy, explosion and reperfusion of the left lung was conducted for 2 hours. As for I/R group,Blood perfusion and ventilation of the left lung were occluded for 1 hour followed by reperfusion for 1 hour. As for CAP group, captopril was injected into the abdominal of rats between the end of ischemia and the beginning of reperfusion ; the other procedures were identical to I/R group. Small pieces of lung tissue were cut after 1 hour reper- fusion. The concentrations of myeloperoxidase （MPO）, malondialdehyde （MDA）, superoxide dismutase （SOD）, expression of ACE mR- NA in lung homogenate and endothelin-1 （ET-1）in serum were determined. The wet to dry weight ratio（W/D） of lung ~vas also measured at the end of reperfusion. The lung tissue was prepared for light microscopic morphological observation at the end of experiment. Results The expression of ACE mRNA was obviously decreased in CAP group than that in I/R group （ P 〈 0.05 ）. The levels of MPO and MDA in lung tissue became significantly lower in CAP group than that in I/R group i P 〈 0.05 ）. The W/D ratio was significantly lower in CAP group than that in I/R group （P 〈 0.05）. The level of ET-1 in serum became significantly lower in CAP group compared with I/R group （ P 〈 0.05 ）. The level of SOD in serum became significantly higher in CAP group than that in I/R group. The lung histological examina- tion showed that lung injury in I/R group was significantly more severe than that in CAP group. Conclusions Captopril postconditioning can significantly reduce lung ischemia-reperfusion injury. The possible mechanism is that captopril postconditioning may inhibit the ex- pression of ACE mRNA in the lung tissue.