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作 者:付新平[1] 张凯伦[1] 叶世铎[1] 蓝鸿钧[1] 邵友梅
出 处:《心肺血管病杂志》1995年第4期198-199,207,共3页Journal of Cardiovascular and Pulmonary Diseases
摘 要:根据冷停搏液不同的灌注途径,18只犬等分成三组:组Ⅰ为主动脉灌注,组Ⅱ右房灌注,组Ⅲ主动脉灌注加冠状静脉窦堵塞。主动脉阻断1h,同时阻断左前降支。结果表明,组Ⅰ梗阻的左前降支辖区心肌组织有氧代谢标志酶-琥珀酸脱氢酶(SDH)活性明显降低,无氧糖酵解标志酶(LDH)活性增强。心肌纤维和线粒体水肿明显。组Ⅱ和组ⅢSDH活性高,LDH活性正常,心肌超微结构基本正常。由此表明,存在左前降支梗阻时,右房灌注和主动脉灌注加冠状静脉窦堵塞增加对缺血心肌超微结构和酶功能的保护。Experimental observations were made in 18 dogs. According to different perfusion routes of cold cardioplegia adopted, the 18 dogs were equally divided into 3 groups: GroupⅠ received aortic perfusion,Group Ⅱright atrial perfusion, GroupⅢaortic perfusion combined with coronary sinus occlusion. The aorta and left anterior descending branch were clamped for one hour. The results indicated that the activities of succinate dehydrogenase (SDH) decreased significantly and these of lactic dehydrogenase(LDHI) increased in the occluded LAD region in GroupⅠ. Edema of myocardial fibers and mitochondria was obvious. On the contrary, SDH activity was higher and LDH activity was normal in GroupⅡ and GroupⅢ .The myocardial ultrastructures were found normal. It suggested that right atrial perfusion and aortic perfusion with coronary sinus occlusion increased the protective effect on ischemic myocardium .
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