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大鼠门静脉动脉化成功治疗四氯化碳诱导的急性肝衰竭

Successful treatment of CCL4-induced acute liver failure with portal vein arterialization in the rat.

作者信息

Nardo B, Puviani L, Caraceni P, Pacilè V, Bertelli R, Beltempo P, Cavallari G, Chieco P, Pariali M, Pertosa A M, Angiolini G, Domenicali M, Neri F, Tsivian M, Bernardi M, Cavallari A

机构信息

Department of Surgery and Transplantations, S. Orsola-Malpighi Hospital, University of Bologna, Italy.

出版信息

Transplant Proc. 2006 May;38(4):1187-9. doi: 10.1016/j.transproceed.2006.03.056.

DOI:10.1016/j.transproceed.2006.03.056
PMID:16757302
Abstract

INTRODUCTION

Optimization of the conditions for regeneration of the native diseased liver is a major goal in patients with acute liver failure. This study sought to determine whether portal vein arterialization (PVA), which increases the oxygen supply to the liver, was protective in a rat model of liver failure.

METHODS

At 24 hours after CCl(4) intoxication, Sprague-Dawley rats (six per group) were assigned to receive PVA or as controls. We determined blood tests, histology, and 10-day survivals. Hepatocyte regeneration was assessed by the mitotic index and bromodeoxyuridine (BrdU) incorporation.

RESULTS

Serum transaminases were significantly lower in PVA-treated rats than in control animals: liver necrosis resolved rapidly after PVA. The BrdU staining and mitotic index were severalfold higher among PVA-treated than in untreated rats. Survival was 100% among rats with PVA and 40% in untreated animals (P < .01).

CONCLUSIONS

PVA led to resolution of CCl(4)-induced massive liver necrosis in the rat. This effect was probably mediated by activation of rapid and extensive hepatocyte regeneration. PVA might provide a novel, alternative approach to treat acute liver failure.

摘要

引言

优化天然病变肝脏的再生条件是急性肝衰竭患者的主要目标。本研究旨在确定增加肝脏氧供应的门静脉动脉化(PVA)在肝衰竭大鼠模型中是否具有保护作用。

方法

在四氯化碳中毒24小时后,将Sprague-Dawley大鼠(每组6只)分为接受PVA组或作为对照组。我们测定了血液检查、组织学和10天生存率。通过有丝分裂指数和溴脱氧尿苷(BrdU)掺入评估肝细胞再生。

结果

PVA治疗的大鼠血清转氨酶显著低于对照动物:PVA后肝坏死迅速消退。PVA治疗的大鼠中BrdU染色和有丝分裂指数比未治疗的大鼠高几倍。PVA大鼠的生存率为100%,未治疗动物的生存率为40%(P <.01)。

结论

PVA导致大鼠四氯化碳诱导的大规模肝坏死消退。这种作用可能是由快速和广泛的肝细胞再生激活介导的。PVA可能为治疗急性肝衰竭提供一种新的替代方法。

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