Bernd Limberg

Beneficial effect of somatostatin on galactosamine induced liver injury

The purpose of our investigation was to study the effect of somatostatin on acute experimental liver injury induced in rats by galactosamine (1.2 g/100 g body wt.). Somatostatin (125 micrograms/100 g body wt.) was administered subcutaneously in a protamine sulphate/ZnCl2 suspension either 2 h prior to the injection of galactosamine or 2 h and again 12 h following the injection. Serum transaminases (GOT, GPT) and serum concentrations of triiodothyronine and thyroxine were determined 28 h after the injection of galactosamine. Histology of the liver was performed by light microscopy. Our results showed that the administration of somatostatin significantly (P less than 0.02) reduced the elevation of GOT and GPT activity and diminished the degree of necrosis, and that although the administration of dibutyryl-cAMP (5 mg/100 g body wt.) intensified galactosamine induced liver injury, this effect of dibutyryl-cAMP could be completely prevented by somatostatin treatment. There was no difference in the serum concentrations of triiodothyronine and thyroxine in controls as compared to galactosamine and galactosamine plus somatostatin treated rats. At present the mechanism of this cytoprotection by somatostatin is unknown.

Somatostatin: A New Therapeutic Agent for Treatment of Hepatic Encephalopathy?

In advanced cirrhosis of the liver Fischer et al. (1975) have described distinctive patterns of amino acids; the aromatic amino acids phenylalanine and tyrosine are elevated and the branched chain amino acids valine, leucine and isoleucine are decreased, therefore the ratio of the molar concentrations of branched chain to aromatic amino acids is reduced. It has been suggested that this amino acid imbalance causes hepatic encephalopathy, since the branched chain and aromatic amino acids compete for entry across the blood-brain barrier. As a consequence of the reduced amino acid ratio the concentrations of aromatic amino acids in the brain increase and lead to elevated levels of false neurotransmitter substances such as octopamine and phenylethanolamine (Smith et al. 1978; James et al. 1976). In cirrhosis of the liver insulin (IRI) and glucagon (IRG) levels are elevated. It has been suggested that the increased glucoregulatory hormones are responsible for the amino acid imbalance and the catabolic state in advanced liver cirrhosis. (Soeters and Fischer 1976).