THE NO DONOR SODIUM-NITROPRUSSIDE REVERSES THE NEGATIVE EFFECTS ON HEPATIC ARTERIAL FLOW-INDUCED BY ENDOTOXIN AND THE NO SYNTHASE INHIBITORL-NAME

In previous studies we have observed that the nitric oxide synthase in hibitor L-NAME induces a profound deterioration of liver circulation i n experimental endotoxemia. Using the same porcine model we now have e valuated the possibility of modulating these effects with the nitric o xide donor sodium nitroprusside. Infusion of endotoxin led to a gradua l deterioration of hemodynamic parameters, including liver blood flow. The decreases in portal blood flow paralleled and matched the decreas es in cardiac output, and no compensatory increase in hepatic arterial flow occurred. L-NAME had detrimental effects on hemodynamics, includ ing the liver circulation. The latter effects could, however, partiall y be reversed by sodium nitroprusside. Hepatic arterial flow increased from 1.9 to 7.2 ml/kg/min, with a concomitant decrease in hepatic art erial resistance from 5,364 to 1,746 dyn s/cm(5) kg. A control group e xhibited no significant change in either flow or resistance. The respo nse to sodium nitroprusside was rapid and vigorous, and probably large ly due to relaxation of the hepatic arterioles, and not to abatement o f intrahepatic edema or plugging of the sinusoids. Furthermore, we con clude that the endotoxin-induced dysfunction of the hepatic arterial b uffer response may be due to a selective inhibition of vascular endoth elial function.