苯那普利后处理减轻离体心脏缺血再灌注损伤的观察

目的探讨苯那普利后处理对大鼠离体心脏缺血再灌注损伤的影响及其机制。方法应用Landendorff装置建立大鼠离体心脏缺血再灌注模型。将24只SD大鼠随机等分为3组：缺血再灌注组（I／R）、缺血后处理组和苯那普利后处理组。生化法检测各组稳灌20min和再灌60min肌酸激酶（CK）的水平，改良亮绿变色酸法观察心肌损害程度，硝基还原酶法测定各组再灌注末一氧化氮（NO）含量，测定心肌组织丙二醛（MDA）含量。结果与缺血再灌注组相比，苯那普利后处理组心肌梗死面积缩小（14±7）％比（40±7）％，P〈0．01]；再灌注流出液中CK含量减少（100．8±31．8）U／ml比（188．5±49．1）U／ml，P〈0．01]；心肌MDA含量降低（2．5±0．7）nmol／mg prot比（4．4±0．6）nmol／mg prot，P〈0．01）；苯那普利后处理组再灌注流出液中NO含量明显高于缺血再灌注组（101．7±8．7）μmol／L比（27．8±5．9）μmol／L，P〈0．01]。结论苯那普利后处理具有显著的心肌保护作用，这种心脏保护作用可能与增加NO浓度和抗脂质过氧化有关。

Benazepril postconditioning attenuates isehemia/reperfusion injury in isolated rat heart

Objective To explore the effects of Benazepril posteanditioning on isehemia/repeffusion injury in isolated rat heart and investigate the possible mechanism. Methods Twenty-four male Sprague-Dawley rats were isolated and perfused using the Langendorff mode with modified Kreb-Henseleit （KH） buffer and were randomly assigned into three groups： I/R group, posteonditioning group, benazepril posteonditioning group. The level of nitric oxide（NO） in the coronary effluent by speetrophotometry and the level of ereatine kinase（CK）in the coronary effluent by biochemistry at the minute of perfusion 20 rain and reperfusion 60 rain. Myocardial infarction size was examined by Gonori chromotropie acid staining（GCA）. The concentrations of MDA were determined. Results Compared with I/R group, myocardial degeneration reduced （14±7）% vs （40±7）%, P〈0.01 ], the level of CK was lower than in I/R group （100.8±31.8）U/ml vs （188.5±49.1）U/ml, P〈0.01], the level of NO was higher （101.7±8.7）μmol/L vs （27.8±5.9）μmol/L, P〈0.01 ], the eoneentrations of MDA was deereased （2.5±0.7） nmol/mg p rot vs （4.4±0.6）nmol/mg p rot, P〈0.01 ] in Benazepril posteonditioning group. Conclusion Benazepril posteonditioning attenuates isehemia/reperfusion injury in isolated rat heart. The possible mechanism might be related to inerease the concentration of NO and antilipid peroxidation.