肝素对心肺复苏后大鼠心肌MDA含量和SOD活性的影响

摘要

目的 观察肝素对心肺复苏后大鼠心肌氧自由基的影响.方法 健康雄性SD清洁级大鼠70只,随即分为三组:假手术组(A组,n=10),心脏骤停盐水组(B,n=30),心脏骤停肝素组(C,n=30),B组和C组又分为30min、2h、6h亚组,每组10只,A组不建立心肺复苏模型,只做手术和气管插管,B和C组建立心肺复苏模型,B组复苏后即刻给予肾上腺素,C组给予肾上腺素和肝素的合剂.自主循环恢复(ROSC)后30min、2h、6h后取心脏测心肌组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性.同时记录心搏骤停时间,自主循环恢复时间和复苏成功率.结果 两复苏组心跳骤停时间差异无统计学意义(P＞0.05),自主循环恢复时间有统计学意义(P＜0.05),复苏成功率B组和C组分别为93.3％和86.7％ (P ＞0.05).复苏后两复苏组心肌MDA含量都升高,与A组比较差异有统计学意义(P＜0.05),其中两组复苏后2h MDA升高最明显,复苏后6h逐渐恢复,B组MDA含量高于C组(P＜0.05).复苏后两复苏组心肌MDA含量都升高,与A组比较差异有统计学意义(P＜0.05),其中两组复苏后2h MDA升高最明显,复苏后6h逐渐恢复,B组MDA含量高于C组(P＜0.05).结论 心肺复苏后2h心肌再灌注损伤最重,复苏开始即刻肝素抗凝能减轻心脏骤停后心肌MDA生成,增加SOD活性,对心肺复苏后大鼠心肌再灌注损伤有一定的保护作用.%Objective To observe the effect of heparin on post - CPR myocardial oxygen radicals in cardiac arrest in rats. Methods 70 healthy SD - cleaned male rats were randomly divided into 3 groups; pseudo surgery group (Group A, n = 10) , saline group with cardiac arrest (Group B, n =30) and heparin group with cardiac arrest ( Group C, n = 30) . Group B and C were further divided into subgroups according to time which was 30 minutes, 2 hours, 6 hours respectively. CPR model was not set up in group A which was just operated on and trachea - intubated. CPR models were established in group B and C. Epinephrine was given to group B after CPR while the mixture of epinephrine and heparin was given to group C. The content of myocardial ma-londialdehyde (MDA) and the activity of the superoxide dismutase (SOD) were tested at 30 minutes, 2 hours and 6 hours after the recovery of spontaneous circulation ( ROSC ) . Meanwhile, we recorded the time of cardiac arrest, the time of spontaneous circulatory recovery and successful recovery rates. Results For the two resuscitation groups, the time of cardiac arrest had not statistically significant difference (P＞0. 05) , while the time of spontaneous circulatory recovery showed significant difference (P ＜0.05). Successful recovery rates in group B and C were 93. 3% and 86. 7% respectively. The content of MDA increased in group B and C( P ＜ 0.01) while the activity of SOD decreased (P ＜ 0. 01). The content of MDA in heparin group decreased significantly than that in routine group at 30 minutes, 2 hours, 6 hours after CPR( P ＜ 0. 01). The activity of SOD in group B and C did not change significantly in 30 minutes aftei CPR(P＞0.05). However, the activity of SOD in heparin group was higher than that in routine group (P ＜0.05) at 2 and 6 hours respectively. Conclusion The cardiac reperfusion injury is the most severe at 2 hours after CPR. Heparin can reduce the production of MDA and increase the activity of SOD when it is given just after CPR begins. Thus, timely heparin intervention plays a certain protective role in cardiac reperfusion injury after CPR.