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体外循环术中心肌缺血 |
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陈伟民 朱洪生 黄日太 蒋为宏 费虹明
【摘要】 目的 研究体外循环术中心肌缺血-再灌注(I-R)损伤后肌浆网Ca2＋调节蛋白mRNA表达。方法 实验用犬12只，主动脉阻断缺血60 min、继之开放后再灌注60 min，建立体外循环术中全心缺血-再灌注心肌损伤模型。于主动脉阻断期间，分组以冷晶体液停跳液间断灌注(ICCC)或温血停跳液持续灌注(CWBC)做心肌保护。采用RT-PCR技术，测定SR Ca2＋-ATP酶、钙螯合蛋白的mRNA水平，观察心输出量(CO)/左室收缩末期压(LVESP)两项心功能指标和心肌细胞超微结构的变化。结果 与缺血前比较，再灌注60 min后：①ICCC组两种蛋白mRNA均显著上升(P＜0.01)，CWBC组无显著变化(P＞0.05)；②两组CO/LVESP均显著下降(P＜0.01)，但组间比较，ICCC组下降更为明显（P＜0.01)；③ICCC组心肌细胞出现超微结构破坏性改变，CWBC组超微结构保持良好。结论 体外循环术中心肌I-R损伤后早期，心肌细胞肌浆网Ca2＋调节蛋白发生了损伤后的分子修复；这种修复可能与心肌损伤程度呈相关。
【关键词】 缺血-再灌注 心肌 SR Ca2＋-ATP酶 钙螯合蛋白 RT-PCR mRNA
mRNA expression of sarcoplasmic reticulum calcium regulatory proteins in myocardium from ischemia-reperfusion injury during cardiopulmonary bypass
Chen Weimin Zhu Hongsheng Huang Ritai
（Department of Cardiothoracic Surgery, Renji Hospital, Shanghai Second Medical University, Shanghai 200001）
【Abstract】 Objective To investigate mRNA expression of sarcoplasmic reticulum (SR) calcium regulatory proteins in myocardium from ischemia-reperfusion (I-R) injury during cardiopulmonary bypass (CPB). Method In 12 anaesthetized canines, animal model was established by aortic crossclamping (AXC) for 60 min, subsequently decrossclamping and reperfusing for 60 min. During the period of AXC, 6 canines received continuous warm blood cardioplegia (CWBC n=6), 6 canines received intermittent cold crystal cardioplegia (ICCC n=6). Levels of mRNA encoding SR Ca2＋-ATPase and calsequenstrin were measured by using reverse transcription-polymerase chain reaction (RT-PCR), cardiac function (cardiac output. CO and left ventricular end systolic pressure. LVESP) assessments were made, and ultrastructure changes of myocardium were observed at two time points: before AXC at baseline, at 60 min of reperfusion after decrossclamping.Results Compared with before AXC at baseline, it was fund that at 60 min of reperfusion: ① SR Ca2+-ATPase and calsequenstrin mRNA levels significantly increased in I[1] [2] [3] 下一页
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