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Heterotopic Auxiliary Liver Transplantation with Portal Flow

机译:门静脉血流异位辅助肝移植

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One of the causes of auxiliary liver transplantation failure is the inter-liver competition between the hostliver and the graft for the hepatotrophic factors of the portal blood. We have developed an experimentalmodel of heterotopic partial (30%) liver isotransplant using Wistar rats so as to study this competition.Splenoportography and dissection demonstrate the existence of collateral circulation. The collateralsat 90 days post-transplant (PT) consisted of veins from the portal vein to the host liver (PR),paraesophageal veins (PE) and splenorenal veins (SR). At 60 days P.T., PR and SR veins but not PEones appeared, and at 30 days P.T., there were only PR veins. Graft atrophy at 90 days P.T. wasassociated with a severe degree of bile duct proliferation.The gradual development of portal hypertension causes porto-systemic collateral circulation and thegraft loses the portal hepatotrophic factors. The late development of the portal hypertension and thebiliary proliferation could be caused by the hepatic arterial ischemia in this experimental model. Thus,as has been described in the orthotopic liver tansplantation, the heterotopic one might require a doublevascularization, both portal and arterial.
机译:辅助肝移植失败的原因之一是宿主肝脏和移植物之间的肝内竞争对门静脉血的肝营养因子的影响。为了研究这种竞争,我们开发了一种使用Wistar大鼠的异位部分(30%)肝脏同种异体移植的实验模型。脾静脉造影和解剖证实了侧支循环的存在。移植后90天(PT)的侧支由门静脉到宿主肝脏的静脉(PR),食管旁静脉(PE)和脾肾静脉(SR)组成。在P.T. 60天时,出现PR和SR静脉,但没有出现PEones;在P.T. 30天时,仅出现PR静脉。移植后90天的萎缩门静脉高压症的逐步发展引起门体系统侧支循环,移植物失去了门静脉肝营养因子。在该实验模型中,肝动脉缺血可能导致门脉高压的晚期发展和胆道增生。因此,如原位肝移植中所述,异位移植可能需要门脉和动脉的双重血管形成。

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