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

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

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.

MeSH terms

  • Alanine Transaminase / blood
  • Animals
  • Aspartate Aminotransferases / blood
  • Carbon Tetrachloride Poisoning / surgery*
  • Disease Models, Animal
  • Liver Circulation*
  • Liver Failure / surgery*
  • Liver Function Tests
  • Male
  • Portal Vein / surgery*
  • Prothrombin Time
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Aspartate Aminotransferases
  • Alanine Transaminase