论文部分内容阅读
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。
OBJECTIVE: To observe the changes of key enzyme activities in cardiac glycometabolism after cardiopulmonary resuscitation (CPR) to investigate the causes and specific mechanisms of myocardial energy metabolism after cardiopulmonary resuscitation (CPR). Methods: Tracheal clamping asphyxiation method was used to establish a rat cardiac arrest model. Randomized groups: 1) normal control group, only surgical operation, did not induce cardiac arrest; 2) 2H group (PR2H group) after resuscitation; and 3) 24H group (PR24H) after cardiopulmonary resuscitation. Myocardial energy metabolism was detected by HPLC, and mitochondrial metabolic enzyme activity was detected by microplate reader. Results: Compared with the control group, the activities of hexokinase (HK) and pyruvate kinase (PK) did not change significantly before and after resuscitation. The activity of phosphofructokinase (PFK) decreased at 24 hours after resuscitation (P <0.05). After 2 hours of resuscitation, the activities of pyruvate dehydrogenase (PDH) and citrate synthase (CS) were significantly decreased (P <0.01), both of them returned to normal 24 hours after resuscitation; Both enzyme (IDH) and α-ketoglutarate dehydrogenase (α-KGDH) enzyme activities decreased 2 hours after resuscitation (P <0.05), but resumed 24 hours after resuscitation. Conclusion: The decrease of key rate-limiting enzyme activity after resuscitation may be one of the causes of myocardial energy metabolism after cardiopulmonary resuscitation.