EFFECT OF ANTIPHLOGISTICS ON THE LEVEL OF BLOOD GLUCOSE IN THE RAT

Abstract

It is well-known that antiphlogistics such as salicylates and pyrazolon derivatives have the multiple effects on tissue metabolism. These metabolic effects including inhibition of corticosteroid biotransformation, uncoupling of oxidative phosphorylation, glycogenolysis, alteration of electrolyte balance and inhibition of mucopolysaccharide biosynthesis seem to merit attention in relation to their antiphlogistic activities (1-3). Tanabe and his co-workers (4, 5) have shown that a death caused by larger doses of phenylbutazone and 5-n-butyl-l-cyclohexyl-2, 4, 6-trioxoperhydropyrimidine (BCP) is probably due to the decompensation of adrenocortical function, since repeated administrations of these agents produce the diffuse hemorrhage and proliferation of adrenal cortex in the rat. Korus et al. (6) have reported that in the inactivation process of cortisone phenylbutazone not only inhibits the transformation of the α, β-unsaturated ketonic group of ring A, but also the degradation of the α-ketolic side chain of ring D. However, Dirscherl and Lutzmann (7) have observed only the inhibitory effect of aminophenazone on the reduction of ring A. These studies imply that the retardation of cortisone biotransformation is a possible component of the antiphlogistic action of these drugs. Ban (8) has emphasized that the site of stimulating action of aminopyrine is located in the hypothalamus. The hyperglycemic effects of morphine (9, 10) and salicylates (11) have been shown to be dependent on the release of catecholamines from the adrenal medulla presumably through the activation of the sympathetic centers in the brain. Therefore, it is conceivable that antiphlogistics such as aminopyrine, phenylbutazone, BCP and indomethacin modify the carbohydrate metabolism through the adrenal functions. The present experiment is an attempt to discover the effects of single and repeated administration of these antiphlogistics on the level of blood glucose in the rat.