论文部分内容阅读
目的 :建立冷挛缩模型 ,探讨冷挛缩对未成熟心肌功能、能量代谢与超微结构的影响。方法 :在离体工作心模型基础上 ,30只新西兰幼兔 ( 3～ 4周 )随机分成三组 : 组 (对照组 ,n =10 ) , 组 (冷挛缩组 ,n =10 ) , 组 (冷挛缩 +低钙心肌保护液组 ,n =10 )。离体缺血再灌注复苏 ,测试缺血前、后心功能 ,心输出量 ,左室收缩压 ,左室舒张末压 ,最大压力变化速率 ,缺血后冠状静脉窦流出液乳酸脱氢酶 ( L DH) ,肌酸激酶 ( CK) ,心肌组织水含量 ,三磷酸腺苷 ( ATP)、二磷酸腺苷、一磷酸腺苷含量 ,电镜观察缺血后心肌超微结构。结果 :离体心缺血再灌注复苏后 ,心功能恢复、电镜观察缺血后超微结构 、 组优于 组 , 、 组 ATP含量始终高于 组 ( P <0 .0 5 ) ,而 组 L DH、CK和心肌组织水含量高于 、 组 ( P <0 .0 5 )。结论 :冷挛缩对缺血后心功能恢复和能量代谢不利 ,低钙心肌保护液有利于减轻冷挛缩损伤
Objective: To establish a cold contracture model to investigate the effects of cold contracture on immature myocardial function, energy metabolism and ultrastructure. Methods: Thirty New Zealand rabbits (3-4 weeks) were randomly divided into three groups: control group (n = 10), cold contracture group (n = 10) Cold contracture + low calcium cardioplegia group, n = 10). In vitro ischemia-reperfusion resuscitation, cardiac function, cardiac output, left ventricular systolic pressure, left ventricular end-diastolic pressure, maximum rate of pressure change, ischemic coronary sinus effluent lactate dehydrogenase ( L DH), creatine kinase (CK), myocardial tissue water content, adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate content and electron microscopy. Results: After revascularization of isolated heart, the cardiac function recovered and the ultrastructure of the ischemic tissue was observed by electron microscopy. The content of ATP was always higher in the group than in the group (P <0.05) DH, CK and myocardial tissue water content was higher than that of the control group (P <0.05). CONCLUSION: Cold contracture is unfavorable to the recovery of cardiac function and energy metabolism after ischemia, and hypocalcemic cardioprotective solution is beneficial to relieve the cold contracture injury