中文摘要：

目的：观察心肺复苏后心肌糖代谢关键酶活性的变化,以探讨心肺复苏后心肌能量代谢障碍的原因和具体机制。方法：采用气管夹闭窒息法,建立大鼠心跳骤停模型。随机分组：1）正常对照组,仅手术操作,不诱导心跳骤停;2）复苏后2H组（PR2H组）;3）心肺复苏后24H组（PR24H）。高效液相色谱检测心肌能量代谢情况,酶标仪检测线粒体代谢酶活性。结果：与对照组相比,己糖激酶（HK）和丙酮酸激酶（PK）在复苏前后酶活性无明显变化;磷酸果糖激酶（PFK）酶活性于复苏后24小时下降（P〈0.05）;心肺复苏2小时后丙酮酸脱氢酶（PDH）酶活性和柠檬酸合酶（CS）酶活性明显下降（P〈0.01）,两者均于复苏后24小时逐渐恢复正常;异柠檬酸脱氢酶（IDH）和α-酮戊二酸脱氢酶（α-KGDH）酶活性均于复苏后2小时下降（P〈0.05）,但复苏后24小时仍未恢复。结论：复苏后糖代谢关键限速酶活性的降低,可能是导致心肺复苏后心肌能量代谢障碍的原因之一。

英文摘要：

Objective：To investigate the enzymes activity of glucose metabolism after restoration of spontaneous circulation（ROSC）, in an effort to explore the potential pathophysiological mechanism of impaired myocardial energy metabolism after cardiopulmonary resuscitation（CPR）. Methods： Cardiac arrest was induced by asphyxia. Animals were randomized into three groups ：（1） sham control group;（2） PR2 H group;（3） PR24 H group. The contents of myocardial high-energy phosphates were measured by high performance liquid chromatography（HPLC）. The spectrophotometer was used to detect glucose metabolic enzyme activity. Results： Compared with control group,activities of hexokinase（HK） and pyruvate kinase（PK） did not chang after ROSC. Activity of phosphofructokinase（PFK） fell only in PR24H（P〈0.05）. Activities of pyruvate dehydrogenase（PDH） and citrate synthase（CS） fell in PR2 H and recovered in PR24H（P〈0.05）. However, activities of isocitrate dehydrogenase（IDH） and α-ketoglutarate dehydrogenase（α-KGDH） fell in PR2H（P〈0.05） but not recovered in PR24 H. Conclusions： The declination of several important key enzymes activities of myocardial glucose metabolism implicates a principal mechanism of impaired myocardial energy metabolism after CPR.