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不同原因诱导大鼠腹主动脉移植硬化的组织病理比较

Histopathology of rat aortic transplant arteriosclerosis induced by different risk factors
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摘要 目的 :研究不同原因诱导的大鼠腹主动脉移植硬化的组织病理学改变。方法 :140只大鼠随机分组 :A组为非移植组 ,B组为同品系移植缺血小于 30min组 ;C组为同品系移植缺血 4h组 ;D组为异品系移植缺血小于 30min组。术后 7、15、30、6 0天切取植入的腹主动脉进行光镜、电镜检查。结果 :移植 7~ 15天时C组动脉内膜有多量多形核粒细胞和单个核细胞粘附、浸润 ,电镜检查多形核粒细胞为中性粒细胞。而D组移植动脉各层均有大量的淋巴细胞浸润。移植 30~ 6 0天时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 :中性粒细胞在缺血 /再灌注损伤诱导的同品系大鼠腹主动脉移植硬化发挥了重要作用 ,其机制值得进一步研究。 Purpose To investigate the histopathology of rat aortic transplant arteriosclerosis induced by different cause. Methods One hundred and forty inbred SD and Wistar rats were randomly divided into the nontransplanted control group (A), the ischemia control group of isografts (B), the ischemia experimental group of isografts (C), the allografts group (D). Grafts were harvested at 7, 15, 30, 60 days after transplantation and studied by light and electron microscopy. Results At the early observation time after transplantation, the cell composition found in the intima of the syngenic vessels with 4 hours of ischemia time consisted of neutrophils and monocytes. Whereas in allogeneic grafts it contained lymphocytes and monocytes. Dominant intimal thickening was found in allogeneic grafts and syngenic grafts with 4 hours of ischema time during the late observation time. The thickening neointimae consisted mainly of monocyte/macrophage and smooth muscle cells (SMC). Conclusions The damage due to prolonged cold ischemia time is sufficient to cause pronounced graft arteriosclerosis. The pathophysiological mechanism leading to ischemia induced arteriosclerosis is different from the one seen in the allogeneic situation.
出处 《临床与实验病理学杂志》 CAS CSCD 2001年第6期515-518,共4页 Chinese Journal of Clinical and Experimental Pathology
基金 广东省中医药管理局基金资助 (No 972 5 6 )
关键词 再灌注损伤 腹主动脉移植硬化 组织病理学 reperfusion injury transplant arteriosclerosis aorta, abdominal rats
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  • 1clemens M,Wittrin C.Bilhamie und Hamobilie nach Reitunfall.Vortrag 66. Hamburg: Tagung Nondwestdeutscher chirurgen, 1975.
  • 2Glaser K, Wetscher G, Pointner R, et al. Traumatic Bilhemia, Surgery, 1994, 116 (l): 24.
  • 3Blum M, Fiedler C, Winde G, et al. Die Billemeamie- ein uberblick ube r Diagnostik und Therapie. Chirurg, 1987, 58:482.
  • 4Enneker C,Berens JP. Schwerste Lebemuptur mit Lebervenenabriss und massive Bilhamie. Chirung,1978, 49:311.
  • 5Reimund KP, Weis C, Bruckner R, et al. Die Bilhamie- eine seltene kom likation nach schwester lebemuptur. Langenbecks Arch chir, 1990. 375:330.
  • 6Soehendia N. Wemer B. Zur Diagnosik der traumatischen Homobilie un d Bilhamie. Disch Med Wochenschr, 1977, 102:428.
  • 7Briani GF, Dederzoli P, Orcalli F, et al. Bilhemia:diagnosietratta nento conservativo a proposito di un caso complicato con ascesse epatic o. Chir Jtal, 1983,35:965.
  • 8Paul LC, Fellstrom B. Chronic Veseular rejection of the heart and the kidney: have rational trealaxem options emerged? Transplantation, 1992, 53:1169.
  • 9Demetris AJ, Zebre T, Banner B. Morphology of solid organ artefiopathy: identification of pmliferating infimal cell populations. Transplant Proc, 1989, 21:3667.
  • 10Hosenpud JD, Shipley GD, Wanger CR. Cardiac allograft vasculopathy: current comepts, recents developments, and future directions. J- Heart Lung Trans plant, 1992, 11:93.

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