冷缺血损伤对大鼠移植物动脉硬化促发作用  

Long cold ischemic injury induces transplant arteriosclerosis

作　　者：孙文宇[1] 毕研文[1] 周志强[1] 

机构地区：[1]山东大学齐鲁医院,济南250012

出　　处：《中国公共卫生》2008年第10期1218-1219,共2页Chinese Journal of Public Health

基　　金：山东省自然科学基金(2007BN0029)

摘　　要：目的探讨4 h冷缺血损伤对大鼠移植物动脉硬化作用。方法利用同种大鼠胸主动脉腹腔移植模型产生动脉硬化病理改变。实验分为免疫耐受组、免疫耐受冷缺血组、同系冷缺血组和对照组。冷缺血组移植前先将供体胸主动脉放人4℃生理盐水中浸泡4 h。通过马松(Masson)三色染色法估计血管硬化程度和增生平滑肌细胞的分布,免疫组化法测定α-肌动蛋白、增殖细胞核抗原、周期蛋白依赖性激酶1和周期蛋白B1在增生平滑肌细胞中的表达程度。结果冷缺血2组均见明显内膜肥厚,主要表现为内、外膜平滑肌细胞大量增生及纤维化,平滑肌细胞排列较密集、成层状。增殖细胞核抗原、周期蛋白依赖性激酶1和周期蛋白B1在增生平滑肌细胞中均高度表达,且随时间推移和动脉硬化的进展其表达程度愈来愈高。结论4 h冷缺血损伤可促发移植物动脉硬化。Objective To explore the effect of 4 hours cold ischemic injury on allograft arteriosclerosis by means of the rat abdominal aortic aUograft model. Methods Inbred male Wistar rats served as donors and Sprague dawley（SD）male rats as recipients. They were divided into groups of immune tolerance, immune tolerance with cold ischemia, isograft with cold ischemia. The isograft abdominal aortic allograft model was set up. The specimens were treated first and the Masson staining was then taken to observe fibrosclerosis degree and morphology and distribution of smooth muscle cells（VSMC）in the vessels. Immunohistochemistry was used to compare of α - actin, PCNA, CDKI, and CyclinB1 expression in proliferating VSMC of intima and adventitia during different times postoperatively. Results Both cold ischemic groups showed significantly intimal hyperplysia appearing mainly in VSMC, proliferation and fibrosclerosis in infima and adventitia. The α - actin, PCNA, CDK1 and CyclinB1 expressed highly in proliferative VSMC and the expressions remarkedly increased with the times and allograft arteriosclero sis＇ progression. Conclusion Four hours cold isehemic injury can lead to transplant arteriosclerosis.

关 键 词：冷缺血 移植物动脉硬化 平滑肌细胞 

分 类 号：R654.2[医药卫生—外科学]