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.