Prevention of the hemorrhagic hypotension-induced hepatic arterial vasoconstriction by L-arginine and naloxone

The possible involvement of the L-arginine-nitric oxide pathway and endogen ous opioid mechanisms in the hemorrhagic hypotension- (HH) induced changes of hepatic arterial blood flow and vascular resistance was studied in cats. During HH hepatic arterial blood flow was significantly higher both in L-a rginine- and naloxone-treated animals than in controls. Furthermore, HH ind uced a significant increase of the hepatic vascular resistance in the contr ol group, which was prevented by L-arginine or naloxone treatment. Because inhibition of the nitric oxide synthesis by N-G-nitro-L-arginine in normote nsive cats induced a similar increase of the hepatic vascular resistance to that observed during HH in the control group, our results indicate that im pairment of the endothelial function may be responsible for the hemorrhage- induced L-arginine- and naloxone-reversible hepatic arterial vasoconstricti on. This hypothesis is consistent with our previous observations demonstrat ing the development of endothelial dysfunction in the feline hepatic artery during HH.