Alterations of renal arachidonate metabolism in rabbits with D-galactosamine-induced acute hepatic failure

Abstract

Renal arachidonate and prostaglandin metabolism was investigated in the rabbits with D-galactosamine (GalN)-induced acute hepatic failure. Urinary excretion of prostaglandin E₂ (PGE₂) for 24h after intravenous injection of GalN (1g/kg) was significantly elevated in relation to increased plasma levels of norepinephrine and epinephrine. This suggest that the GalN-treated rabbits have compensatory augmentation of the renal synthesis of PGE₂ to maintain renal blood flow against vasoconstrictors. Twenty-four h after GalN-treatment, renal cortical PGE₂ content was significantly smaller than that in non-treated rabbits, suggesting that PGE₂ production in renal cortex was impaired at this stage. Arachidonate content of tissue homogenate was significantly reduced in renal cortex of the GalN-treated rabbits. This may result from consumption of arachidonate by increased renal synthesis of prostaglandins and/or from decrease of its supply from the injured liver.