心脏骤停大鼠自主循环恢复后心肌损伤的特点

The characteristics of myocardial injury in rats resuscitated from cardiac arrest

的明确心脏骤停(cardiac arrest,CA)大鼠自主循环恢复(restoration of spontaneous circulation,ROSC)后心肌损伤的特点及其机制。方法42只雄性Wistar大鼠随机(随机数字法)分为复苏后(post resuscitation,PR)4h组、PR24h组、PR48h组及假手术(sham)组。经皮电刺激心外膜诱导室颤建立大鼠CA模型,CA6 min后开始心肺复苏(cardiopulmonary resuscitation,CPR)。各组动物至观察时间点行超声心动图检测心功能,行正电子发射型计算机断层显像检测心肌葡萄糖代谢最大标准化摄取值(maximum standardized uptake value,SUVmax),测线粒体通透转换孔(mitochondrial permeability transition pore,MPTP)开放程度及线粒体膜电位(mitochondrial membrane potential,MMP),并通过电镜观察心肌超微结构。结果PR4h出现心功能不全,左室射血分数、心输出量下降(均P<0.01),舒张期左室后壁增厚(P<0.01),舒张末左室容量变小(P<0.05),PR48h心超参数与sham组比较差异无统计学意义(P>0.05);与sham组相比,PR4h组心肌SUVmax升高,线粒体吸光度下降明显,MMP降低,差异有统计学意义(均P<0.01),PR48h组上述参数与sham组比较差异无统计学意义(均P>0.05);PR4h及PR24h组心肌线粒体肿胀,线粒体嵴稀疏,但心肌超微结构完整。结论CA/ROSC后发生复苏后心功能不全,但ROSC后48h受损的心功能可完全恢复,其原因可能与心肌损伤为可逆性,线粒体功能和结构逐渐恢复有关。

Objective To investigate the characteristics of myocardial injury and its underlying mechanism in rats resuscitated from cardiac arrest.Methods Forty-two male Wistar rats were randomly(random number)assigned into the post-resuscitation (PR)4h,PR 24h,PR 48h,and sham groups.Ventricular fibrillation was induced by transcutaneous electrical epicardium stimulation and untreated for 6min,followed by cardiopulmonary resuscitation (CPR).Myocardial function,glucose metabolism,myocardial ultrastructure,the status of mitochondrial permeability transition pore (MPTP)and mitochondrial membrane potential (MMP)were evaluated at different time points.Results Myocardial dysfunction was found at 4h after restoration of spontaneous circulation (ROSC).The ejection fraction and cardiac output were decreased (all P<0.01),the diastole left ventricular posterior wall became thicker (P<0.01),and the end-diastolic volume was reduced (P<0.05).However,cardiac function was recovered almost completely at 48h after ROSC.The PR 4h group had a higher SUVmax,a more obvious decreased absorbance,and a lower MMP than the sham group (all P<0.01),but no statistically significant differences were noted between the PR 48h group and the sham group (P>0.05).At 4h and 24h after ROSC,the mitochondria was swollen and the mitochondrial crista was sparse,but the myocardial ultrastructure was complete.Conclusions Post resuscitation myocardial dysfunction occurs after ROSC and the myocardial dysfunction is completely reversible at 48h after ROSC,which may be reIated to the reversibility of myocardial injury and the gradual recovery of mitochondrial structure and fimction.