Local arterial vasoconstriction induced by octreotide in patients with cirrhosis

Peripheral vasodilation initiates the hyperdynamic circulation in cirrhosis . Somatostatin and its analogues, such as octreotide, have a vasoconstricti ve effect in cirrhotic patients and experimental animals with portal hypert ension. The exact mechanism of octreotide-induced vasoconstriction remains unknown. To investigate whether octreotide produces vasoconstriction throug h suppression of vasodilatory peptides, such as glucagon, or through a loca l effect, we evaluated the effect of an intra-arterial dose on forearm bloo d flow (FBF), while measuring systemic glucagon levels. FBF was measured in 10 cirrhotic patients by venous occlusion plethysmography. The brachial ar tery of the nondominant arm was catheterized, and vasoactive drugs were adm inistered: methacholine 4 mu g/min; octreotide 20 mu g/h, and octreotide 20 mu g/h + methacholine 4 mu g/min. Each infusion, lasting 5 minutes, was fo llowed by saline for washout. FBF was measured in both arms during the last minute of each infusion and at the end of washout, with the uninfused arm acting as the control, Nitrates and nitrites, octreotide, and glucagon bloo d levels were determined at baseline and after each infusion. Percent chang e in flow (%Delta) was obtained by comparing the flow during drug administr ation to that during the preceding saline infusion. Saline infusion did not alter FBF, but octreotide infusion resulted in a 34% +/- 7.7 (P < .005;) r eduction in FBF in the infused arm, FBF in the control arm was unchanged de spite a significant decrease in systemic glucagon levels. Methacholine infu sion increased FBF around 300%, which was not altered by the concomitant in fusion of octreotide. Octreotide has a local vasoconstrictive effect that s eems nitric oxide (NO)-independent, Octreotide probably has a facilitating effect over vasoconstrictors increased in chronic liver diseases.