Prostaglandin E1 (PGE1) attenuates vasoconstriction induced by PGE2, PGD2 and phorbol myristate acetate in the perfused rat liver.

It has been shown that prostaglandins (PGs) produced by Kupffer and endothelial cells play an important role in mediating physiological responses to various immunological stimuli. We studied the effect of prostaglandin E1 (PGE1) on the hemodynamic and metabolic changes induced by prostaglandin E2 (PGE2), D2 (PGD2) and phorbol 12-myristate 13-acetate (PMA), a potent inducer of PGs in the isolated rat liver perfused with Krebs-Ringer-bicarbonate (KRB) solution at a constant pressure of 12 cmH2O. The liver was taken from overnight-fasted male Sprague-Dawley rats weighing 260 to 310 g. Both PGE2 and PGD2 significantly decreased hepatic flow when their initial concentration was elevated to micromolar range. Although 1 x 10(-6) M of PGE1 did not have a major effect on hepatic flow, it significantly attenuated the declines of hepatic flow produced by 4 x 10(-6) M of PGE2 and PGD2. However, none of PGs tested influenced glucose and lactate concentrations in the medium. Continuous infusion of PGE1 into the medium at a rate of 5 microg.min(-1) significantly diminished the decreases in hepatic flow and oxygen consumption induced by 2 x 10(-8) M of PMA. These results suggest that administration of PGE1 may preserve hepatic blood flow by modifying the intrahepatic regulatory mechanism involving the activation of Kupffer and endothelial cells.