蛋白激酶C对离体兔心脏的保护作用

目的探讨蛋白激酶C对离体兔心的保护及机制。方法应用蛋白激酶C的激活剂和阻断剂,通过Langendroff离体兔心灌注模型,测定心功能指标、心肌CK-MB、LDH、MDA、SOD含量,计算心肌含水量及检测凋亡细胞,了解蛋白激酶C对心功能的影响。结果缺血预适应组和蛋白激酶C激活组的心肌CK-MB(233·6U/g±24·6U/g,285·9U/g±21·4U/g),LDH(83·9U/g±6·5U/g,91·2U/g±5·4U/g和SOD(201·0U/g±17·4U/g,91·9U/g±22·1U/g)含量均高于对照组(132·5U/g±24·8U/g,74·1U/g±7·4U/g,180·3U/g±16·8U/g)和激活阻断组(135·1U/g±28·8U/g;75·1U/g±8·8U/g,184·5U/g±16·9U/g)(P<0·05),而MDA含量、心肌含水量明显低于对照组和激活阻断组(均P<0·05)。结论蛋白激酶C对离体兔心具有肯定的保护作用。

Protective effect of protein kinase C on heart function: an experiment with isolated rabbit hearts

OBJECTIVE: To investigate the protective effect of protein kinase C on heart function. METHODS: The hearts of 40 rabbits were isolated, underwent Langendorff perfusion, and randomly divided into 4 equal groups: Group I (control group, the heart underwent long ischemia or preservation for I hour, was re-warmed and re-infused, and then re-perfused with K-H fluid), Group II (ischemic preconditioning group, perfusion was stopped for 5 minutes before the long ischemia, then the aorta was re-infused), Group III (specific activator of PKC, phorbol myristate acetate was infused inversely via the aorta before the perfusion of K-H fluid), and Group IV (polymyxin B, a specific antagonist of PKC, was infused after the infusion of PKC). Before the preservation and by the end of reperfusion left ventricle end systolic pressure (LVESP), and left ventricle end diastolic pressure (LVDSP) were measured. At the end of experiment specimens of myocardium were collected from each heart to measure the water content, the levels of lactic dehydrogenase and MB isoenzyme of creatine kinase (CK-MB), superoxide dismutase (SOD), and malonyldialdehyde (MDA). TUNEL method was used to measure the number of apoptotic cardiomyocyte. RESULTS: All heart resumed beating. The LVESP of Group II and III were both significantly higher than those of Groups I and IV (all P < 0.05) and the LVESP of Group III was significantly higher than that of Group II too (P < 0.05). The LVEDP of Group II and III were both significantly lower than those of Groups I and IV (all P < 0.05) and the LVEDP of Group III was significantly lower than that of Group II too (P < 0.05). The levels of CK-MB, LDH, and SOD of Group II and III were all significantly higher than those of Groups I and IV (all P < 0.05) and the levels of CK-MB and LDH of Group III was significantly higher than that of Group II too (P < 0.05). The level of MDA of Group II and III were both significantly lower than those of Groups I and IV (all P < 0.05) and the level of MDA of Group III was significantly lower than that of Group II too (P < 0.05). The water contents of Group II and III were both significantly lower than those of Groups I and IV (all P < 0.05). The numbers of TUNEL positive cell and apoptotic cells of Group II and III were all significantly lower than those of Groups I and IV (all P < 0.05). CONCLUSIONS: PKC can be activated by transient ischemia and PMA. PKC protects the heart function effectively.