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目的 :通过检测肌酸磷酸激酶同工酶MB(CK MB)和肌钙蛋白I(cTnI) ,了解无复流时CK MB和cTnI的变化与心肌微血管损害之间的关系 ,分析微血管损伤对CK MB和cTnI释放的影响。方法 :19只犬通过制作急性心肌缺血 再灌注动物模型 ,采用弹丸式注射声学造影剂Albunex进行心肌声学造影研究 ;测定外周循环中CK MB和cTnI在基础状态、6 0min心肌缺血 (T0 )、再灌注 6 0min时的浓度(T60 ) ,计算再灌注 6 0min时其上升斜率 (T60 -T0 6 0 )和相对增加值 (T60 -T0 T0 )。结果 :CK MB和cT nI在心肌缺血 6 0min时外周血液浓度明显高于基础状态 (P <0 .0 1) ,复流组明显高于无复流组 (P <0 .0 1) ;6 0min再灌注时CK MB和cTnI的浓度、上升斜率和相对增加值复流组仍显著高于无复流组 (P<0 .0 1和P <0 .0 0 1)。结论 :心肌微血管床的损害影响缺血再灌注心肌酶和结构蛋白的释放。
OBJECTIVE: To investigate the relationship between changes of CK MB and cTnI and myocardial microvascular damage during no-reflow by detecting creatine phosphokinase MB (CK MB) and cardiac troponin I (cTnI), and to analyze the relationship between microvascular damage and CK Effects of MB and cTnI release. METHODS: Nineteen dogs were subjected to acute myocardial ischemia / reperfusion (I / R) animal model by intracranial injection of Albunex. The MBMC and cTnI in the peripheral circulation were measured at basal state, 60 min myocardial ischemia (T0) (T60) at 60 min after reperfusion, and the rising slope (T60 -T0 60) and relative increase (T60 -T0 T0) at 60 min reperfusion were calculated. Results: The peripheral blood concentrations of CK MB and cT nI at 60 min of myocardial ischemia were significantly higher than those of the basal state (P <0.01). The levels of CK MB and cT nI were significantly higher than those of no - reflow group (P <0.01). The concentration, rising slope and relative increase of CK MB and cTnI at 60 min after reperfusion were still significantly higher in reperfusion group than in no-recovery group (P <0.01 and P <0.01). Conclusion: The damage of myocardial microvascular bed affects the release of myocardial enzymes and structural proteins during ischemia / reperfusion.