目的观察犬心跳骤停复苏后心肌细胞凋亡和氧自由基的变化。方法12只犬随机分为2组,心肺复苏组(cardiopulmo nary resascitation,CPR组)和空白对照组,每组6只,CPR组电击诱发犬心室颤动,3分钟后开始复苏,采用Swan-Ganz漂浮导管监测复苏前和恢复自主循环后0,0.5,1,2,4,6小时的平均动脉压、心输出量和肺动脉楔压,6小时后取心肌组织,TUNEL法检测心肌细胞凋亡,心肌组织匀浆测丙二醛和超氧化物歧化酶的活性。结果两组各血流动力学指标在心跳骤停前无统计学差异,CPR组的平均动脉压在恢复自主循环4小时和6小时低于空白对照组。CPR组的肺动脉楔压从心跳骤停前的(5.0±1.3)mmHg持续上升,到复苏后6小时达到(28.8±4.8)mmHg,各观察点均高于空白对照组,心输出量在复苏成功后随时间延长而下降,6小时降至最低,复苏后各观察点均低于空白对照组。CPR组心肌细胞凋亡明显多于空白对照组。复苏后6小时,CPR组心肌组织丙二醛活性高于空白对照组,而超氧化物歧化酶活性低于空白对照组。结论电击诱发心室颤动犬复苏成功后存在着心功能不全,其可能与复苏后心肌氧自由基的产生和心肌细胞凋亡增加,以及内源性抗氧化机制的削弱有关。 Objective To observe the changes of cardiomyocyte apoptosis and oxygen free radicals in cardiac arrest and resuscitation. Methods 12 dogs were randomly divided into 2 groups: cardiopulmonary resuscitation (CPR group) and blank control group (6 rats in each group). CPR group induced canine ventricular fibrillation (VFV) and started resuscitation after 3 minutes. Swan-Ganz floating The mean arterial pressure, cardiac output and pulmonary artery wedge pressure were measured at 0, 0.5, 1, 2, 4 and 6 hours after resuscitation and recovery of spontaneous circulation. Cardiomyocytes were harvested after 6 hours. Cardiomyocyte apoptosis was detected by TUNEL. Tissue homogenates were tested for malondialdehyde and superoxide dismutase activity. Results There was no significant difference in hemodynamic parameters between the two groups before cardiac arrest. The mean arterial pressure in CPR group was lower than that in control group at 4h and 6h after spontaneous recovery. Pulmonary artery wedge pressure in CPR group increased continuously from (5.0 ± 1.3) mmHg before cardiac arrest to (28.8 ± 4.8) mmHg at 6 hours after resuscitation, and each observation point was higher than that of blank control group Afterward, it decreased with time and dropped to the lowest level in 6 hours. After resuscitation, the observation points were all lower than the blank control group. CPR group myocardial cell apoptosis was significantly more than the blank control group. At 6 hours after resuscitation, the activity of MDA in myocardium of CPR group was higher than that of blank control group, while the activity of superoxide dismutase was lower than that of blank control group. CONCLUSIONS: Insufficient heart function after successful shock resuscitation in shock-induced VF rats may be related to the generation of myocardial oxygen free radicals and the increase of cardiomyocyte apoptosis following resuscitation and the impaired endogenous antioxidant mechanism.