摘要
目的 :研究缺血损伤诱导的同品系大鼠腹主动脉移植硬化的组织病理学改变 ,并探讨其可能机理。方法 :1 4 0只大鼠随机分组 :A组为非移植组 ,B组为同品系移植缺血 <3 0min组 ;C组为同品系移植缺血 4h组 ;D组为异品系移植缺血 <3 0min组。术后 7天、 1 5天、 3 0天、 60天切取植入的腹主动脉进行光、电镜检查。结果 :移植早期C组动脉内膜有多量多形核白细胞和单个核细胞粘附、浸润 ,电镜检查多形核白细胞为中性白细胞。而D组移植动脉各层均有大量的淋巴细胞浸润。移植后期C组、D组移植动脉内膜均有显著增厚 ,增生的内膜均由单核 /巨噬细胞和平滑肌细胞构成 ,但前者无中膜层平滑肌坏死及弹力膜断裂现象。结论 :中性白细胞在缺血 /再灌注损伤诱导的同品系大鼠腹主动脉移植硬化中发挥了重要作用 。
Objective:To investigate the histopathology of aortic transplant arteriosclerosis induced by ischemia in rats.Method:One handred and fourty inbred SD and Wistar rats were randomly divided into the non_transplanted control group A, the ischemia control group of isografts(B),the ischemia experimental group of isografts(C),and the allografts group(D).Grafts were harvested for 7,15,30,60 days after surgery,studied by light and electron microscopy.Result:At the early transplantation,the cell compositions found in the intima of the syngenic vessels with 4 hours of ischemia time consisted of neutrocytes and monocytes.Whereas in allogeneic grafts there contained lymphocytes and monocytes.Dominant intimal thickenings were found in allogeneic grafts and syngenic grafts with 4 hours of ischema time at the late transplantation. The thickening neointimas consisted mainly of monocytes/macrophages and smooth muscle cells.Conclusion:The injury by prolonged hypothermic ischemia time was sufficient to cause pronouced graft arteriosclosis.The pathophysiological mechanism leading to ischemia_induced arterioclosis was different from the one seen in the allogeneic situation.
出处
《汕头大学医学院学报》
1999年第3期6-8,共3页
Journal of Shantou University Medical College