肝素对窒息性心跳骤停-复苏致大鼠心肌损伤的影响

目的 探讨窒息性心跳骤停大鼠心肺复苏时应用肝素抗凝对心肌损伤的影响.方法 健康雌性SD大鼠30只,12～16周龄,体重450～500 g,随机分为3组(n=10):假手术组(S组)、常规心肺复苏组(AD组)和常规心肺复苏+肝素抗凝组(AD+Hep组).制备窒息性心跳骤停模型,窒息8min后行心肺复苏(胸外心脏按压200次/min与药物复苏同时进行,复苏时间2min),AD+Hep组常规药物复苏同时静脉注射肝素0.5 mg/kg(0.1 ml/kg),AD组静脉注射与肝素等容量的生理盐水,S组只行动静脉置管和气管插管.自主循环恢复(ROSC)后2 h,取股动脉血2ml后处死大鼠,取心肌组织,测定血清心肌肌钙蛋白Ⅰ(cTnI)浓度、心肌丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性,电镜下观察心肌超微结构.记录从窒息到心跳骤停时间、心肺复苏开始到ROSC时间.结果 与S组比较,AD组和AD+Hep组心肌MDA含量升高,SOD活性降低,血清cTnI浓度升高(P<0.05或0.01),心肌病理损伤明显.与AD组比较,AD+Hep组心肺复苏开始到ROSC时间缩短,心肌MDA含量降低,SOD活性升高,血清cTnI浓度降低(P<0.05或0.01),心肌病理损伤减轻.结论 窒息性心跳骤停大鼠心肺复苏时应用肝素抗凝可减轻心跳骤停.复苏致心肌损伤,其机制可能与抑制脂质过氧化反应有关.

Effects of heparin on myocardial injury following asphyxial cardiac arrest-resuscitation in rats

Objective To investigate the effects of heparin on myocardial injury induced by asphyxial cardiac arrest-resuscitation in rats.Methods Thirty 12-16 weeks old SD rats weighing 450-500 g were randomly divided into 3 groups (n = 10 each): group Ⅰ sham operation (S) underwent no cardiac arrest;group Ⅱ asphyxial cardiac arrest+ CPR (AD) and group Ⅲ asphyxial cardiac arrest + CPR + heparin (AD + Hep). The animals were anesthetized with intraperiteneal pentubarbital 45 mg/kg, intubated and mechanically ventilated. Asphyxia was induced by occlusion of tracheal tube. Cardiac arrest was confirmed by asystole or ventricular fibrillation or electromechanical dissociation on ECG, MAP < 10 mm Hg and eyanosis. Tracheal occlusion was released after 8 rain asphyxia. Closed cardiac massage (200 compressions/min) was performed and intravenous adrenaline 0.01 mg/kg and sodium bicarbonate 1 mmol/kg was given. Group Ⅲ received heparin 0.5 mg/kg immediately after adrenaline and NaHCO3. Recovery of spontaneous circulation (ROSC) was verified by normal QRS complex on ECG, precordial pulsation, MAP> 60 mm Hg for more than 10 min. Arterial blood samples were taken at 2 h after ROSC for measurement of serum concentration of cardiac treponin Ⅰ (cTnI). Myocardial specimens were obtained for microscopic examination and determination of MDA content and SOD activity. The time intervals from asphyxia to cardiac arrest and between start of CPR and ROSC were recorded. Results The time interval from the start of CPR to ROSC was significantly shorter in AD + Hep group (Ⅲ) than in AD group (group Ⅱ). The myocardial MDA content and serum cTnI concentration were significantly lower and the myocardial SOD activity was significantly higher in group AD + Hep than in group AD. Microscopic examination showed less myocardial damage in group AD + Hep than in group AD. Conclusion Anticoagulation with heparin can attenuate asphyxial cardiac arrest-resuscitation induced myocardial injury through inhibition of lipid peroxidation.