We studied the effects of putrescine on acute liver failure caused in rats by two injections of 1 gmkg D-galactosamine. The hepatic polyamine level rose only slightly in the D-galactosamh&njected rats treated with glucagon and insulin, and ['Hlthymidine incorporation into DNA increased little; these
Protective effects of fibronectin in galactosamine-induced liver failure in rats
✍ Scribed by Takashi Moriyama; Hiromu Aoyama; Shin Ohnishi; Michio Imawari
- Publisher
- John Wiley and Sons
- Year
- 1986
- Tongue
- English
- Weight
- 700 KB
- Volume
- 6
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
The effects of supplementation with fibronectin on liver damage and survival in rats with galactosamineinduced liver failure were studied. In rats with acute liver failure induced by a low dose of galactosamine, supplementation with purified plasma fibronectin at 3 hr after the administration of galactosamine provided significant increase of plasma fibronectin levels and augmentation of reticuloendothelial system function at 4 hr , significantly higher plasma fibronectin levels and significant protection of liver damage with shorter prothrombin times, lower AST and less histological damage at 48 hr as compared to control animals. Plasma fibronectin levels were inversely correlated with both plasma prothrombin times and AST. Fibronectin supplementation at 6 hr also resulted in the significant decrease of liver damage at 48 hr as evaluated histologically. When rats with liver failure, induced by a high dose of galactosamine, were supplemented with fibronectin at 3 hr, the survival rate was significantly higher than that of control rats. The results indicate that fibronectin supplementation in the early stages of acute liver failure could reduce liver damage and improve the survival of rats with galactosamine-induced liver failure.
The reticuloendothelial system function has been reported to be impaired in patients with fulminant hepatic failure (l), and it has been considered to play an important role in the development of the frequently observed complications such as endotoxemia, disseminated intravascular coagulation, sepsis and multiorgan failure (2- 5). In an experimental model of liver failure, the reticuloendothelial system has been shown to be an important factor in the development and progression of the liver failure (6). Thus, the reticuloendothelial system function may play an important role in the genesis of acute liver failure as well as the development of the complications.
We have recently reported decreased levels of plasma fibronectin and impaired Kupffer cell function in patients with fulminant hepatic failure (7,8). In the preliminary study, we have also observed the decrease of plasma
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