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目的 研究冷心脏停搏液心肺转流 (CPB)下犬心肌损伤与c fos基因的表达。方法 10只犬分为实验组 (I组 ,n =6 )和对照组 (II组 ,n =4 )。I组动物施行全身低温心脏深低温 4℃St.Thomas液顺行灌注心停搏CPB ,II组动物在常温下施行不停跳并行循环。取不同时点的右心房组织进行免疫组化分析及透射电镜观察。结果 并行循环前 ,两组动物心肌细胞均无Fos阳性核染色 ;血管内皮细胞均有少量阳性染色。I组主动脉阻断 6 0min、主动脉开放 2 0及 4 0min心肌细胞核Fos阳性率持续增加 ;各时点血管内皮细胞Fos阳性率明显增加 ,且以主动脉开放 4 0min最高。II组并行循环 10 0min时 ,心肌细胞及血管内皮细胞Fos阳性率与并行前比较差异显著 (P <0 0 1) ,而显著低于I组同时点。I组开放主动脉 4 0min时心肌超微结构存在损伤征象。结论 (1)冷心脏停搏液CPB下心肌存在一定的缺血 再灌注损伤 ;缺血和 (或 )低温诱导c fos的表达 ,再灌注则显著诱导心肌c fos的表达 ;(2 )血管内皮细胞c fos表达较心肌细胞迅速和强烈 ;(3)CPB本身亦可能诱导c fos基因的表达 ;(4)c fos表达增加与心肌损伤有关
Objective To investigate the myocardial injury and c fos gene expression in dogs under cardioplegia (CPB) with cold cardioplegia. Methods Ten dogs were divided into experimental group (group I, n = 6) and control group (group II, n = 4). Group I animals underwent systemic hypothermia at 4 ℃ St.Thomas fluid perfusion cardiac arrest CPB, II animals were beating and circulating at room temperature. Right atrial tissue at different time points was examined by immunohistochemistry and transmission electron microscopy. Results Before parallel circulation, there was no Fos positive nuclear staining in both groups of animal cardiomyocytes; a small amount of positive staining was observed in the vascular endothelial cells. In group I, the positive rate of Fos positive cells in myocardial aorta was increased at 60 min, at 20 and 40 min after aorta opening. The positive rate of Fos in vascular endothelial cells at each time point was significantly increased, and the aorta opened at 40 min. In group II, the positive rate of Fos in cardiomyocytes and vascular endothelial cells was significantly different from that in parallel group (P <0.01) at 10 min, but significantly lower than that in group I at 10 min. Myocardial ultrastructures were damaged in the open aorta in Group I at 40 minutes. CONCLUSIONS: (1) Myocardial ischemia-reperfusion injury is induced by cold cardioplegia in CPB; c-fos expression is induced by ischemia and / or hypothermia; however, c-fos expression is significantly induced by reperfusion; (2) (3) CPB itself may also induce the expression of c fos gene; (4) The increase of c fos expression is related to myocardial injury