Hemoperfusion-Induced Respiratory Distress Syndrome in an Animal Model: The Effects of Corticosteroids

Abstract

To facilitate the rational design and evaluation of new therapies for fulminant hepatic failure (FHF) a highly reproducible model of this syndrome has been developed in the rabbit (Blitzer et al. 1978). The selective hepatotoxin, galactosamine hydrochloride (4.25 mmol/kg), is administered intravenously to genetically uniform rabbits. Hepatic coma ensues after a predictable time interval (12–44h) and usually lasts for 2–3 h, the animals dying from FHF associated with diffuse hepatocellular necrosis. The sequential neurologic abnormalities, variations in plasma levels of aminotransferases, ammonia and amino acids, deficiencies of blood coagulation factors and electroencephalographic changes in galactosamine-treated rabbits resemble strikingly corresponding changes observed in FHF in man. Preliminary cross circulation experiments have suggested that this animal model of FHF is reversible (Berk et al. 1980). Indeed, it seems to fulfill each of the five major requirements for an appropriate animal model of FHF proposed by Terblanche et al. (1975), i.e. reversibility, reproducibility, death from liver failure, large animal model and minimal hazard to personnel. This model of FHF appears to be superior to other currently available models (Saunders, 1979).