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对缺血心肌恢复血流灌注已日益成为一项重要的治疗措施。虽然再灌注可以挽救缺血的濒危心肌,但在长时间缺血后,再灌注可以引起出血姓梗塞(hemorrhagic infarct)、心律紊乱以至于心室纤颤及持久的心功能障碍等方面的损害作用。对再灌注性损伤的机制的探讨,除有利于进一步认识该现象的本质外,还具有重要的临床实践意义。一、能量代谢异常1976年,Theroux报道,狗冠脉左旋支结扎2小时后进行再灌注,采用植入性超声晶体测量节段的心肌收缩功能表明,梗塞区周围心肌功能恢复需4周以上。对5至15分钟缺血心肌的再灌注,心肌收缩功能减弱可持续24小
Restoring blood flow to ischemic myocardium has increasingly become an important treatment. Although reperfusion can save ischemic endangered myocardium, reperfusion may cause damage to hemorrhagic infarct, arrhythmia, ventricular fibrillation and long-lasting cardiac dysfunction after prolonged ischemia. The research on the mechanism of reperfusion injury has an important clinical significance in addition to further understanding the essence of the phenomenon. First, abnormal energy metabolism In 1976, Theroux reported that left coronary artery ligation 2 hours after the reperfusion, using implanted ultrasound measurement of segmental myocardial systolic function shows that myocardial infarction around the functional recovery of more than 4 weeks. For 5 to 15 minutes of reperfusion of ischemic myocardium, myocardial contractility weakens for 24 hours