心肺转流下犬心肌c-fos基因的表达

C-fos gene expression of the myocardium during cardiopulmonary bypass in dog

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

Objective To study the c-fos gene expression in the myocardium subjected to cardiopulmonary bypass(CPB) with cold cardioplegic arrest. Methods Ten dogs were randomly divided into two groups. The CPB model was established by simulating the routine clinical regimen completely. Hypothermic CPB with cold(4℃) cardioplegic arrest using St.Thomas' solution was used in group I. Group II served as the control(normothermic CPB with non-cardioplegic arrest).According to the duration of CPB, right atrial biopsy specimens were taken at four time points of before CPB (T 0), 60 min after cross-clamping aorta (T 1), 20 min after declamping aorta(T 2), 40 min after declamping aorta (T 3) in group I and at two time points of before CPB( T 0) and at the end of CPB( T 3 ) in group II.Cryostat sections (samples were postfixed in acetone at -20℃) were stained with polyclonal antibodies according to the peroxidase- antiperoxidase method. Ultrastructure of the myocardium was examined under electron microscope. Results Before CPB, there was no staining for Fos protein in the nuclei of the cardiac myocytes, but there was a few Fos-positive nuclei of vascular endothelial cells in group I and II. In group I, the positive rate was significantly increased in vascular endothelial cells as well as in the cardiac myocytes. In group II, the staining for Fos protein was higher in cardiac myocytes and in vascular endothelial cells at T 3 than that at T 0, but much lower than that at T 3 in group I.In group I, ultrastructure of the myocardium was abnormal at T 3. Conclusion (1) There is an ischemia-reperfusion injury in the myocardium undergoing hypothemic CPB with cold cardioplegic arrest. Ischemia and/or hypothermia may induce the c-fos expression. (2)C-fos gene expression in vascular endothelial cells is stronger than that in the cardiac myocytes after CPB. (3)CPB itself may likely to induce c-fos gene expression. (4) C-fos gene expression is related to myocardial ischemia-reperfusion injury.