Intermittent hepatic dearterialization induces glucose intolerance: an experimental study in the rat.

Intermittent hepatic dearterialization is used in the palliative treatment of liver malignancy. However, its metabolic consequences are not established. Therefore the influences of the procedure on the plasma insulin, glucagon and glucose responses were studied in healthy rats and in rats with a tumour inoculated subcapsularly into the liver. To study the influence on stimulated islet hormone secretion we infused arginine intravenously (7 mg/min) for 30 min, because arginine is known to stimulate the secretion of both insulin and glucagon. During hepatic dearterialization, hyperglycaemia developed; mean(s.e.m.) blood glucose levels after 60 min of dearterialization were 20.2(1.3) mM versus 14.7(1.5)mM in controls (P less than 0.001). Concomitantly, compensatory hyperinsulinaemia and hypoglucagonaemia occurred. Furthermore, during both dearterialization and in the immediate reperfusion phase, the arginine-induced increase in plasma insulin levels was impaired (P less than 0.001), whereas the arginine-induced increase in plasma glucagon levels was not significantly affected. These changes were qualitatively the same in tumour-free and tumour-bearing rats. We conclude that glucose intolerance develops during selective hepatic dearterialization, which is evident both from basal hyperglycaemia and impaired insulin secretion.