[Effects of two different dosages of octreotide on portal pressure and hepatic hemodynamics in cirrhotic portal hypertensive patients after portal-azygous devascularization and splenectomy].

OBJECTIVE: Increased portal inflow and intrahepatic resistance may play a part of the role in pathogenesis of portal hypertension in cirrhotic patients. Some vasoactive substances may play an important role in the regulation of hepatic hemodynamics. The aim of this study is to investigate the effects of two different dosages of octreotide on portal pressure and hepatic hemodynamics.

METHODS: 26 cirrhotic patients who underwent portal-azygous devascularization and splenectomy were investigated in a randomized and double-blind study. Patients were assigned to receive treatment either with a bolus of octreotide 100 microg, followed by infusion of 50 microg/h for 72 h (Group A, n = 12) or with a bolus of octreotide 100 microg, followed by infusion of 25 microg/h for 72 h (Group B, n = 14). The portal pressure was dynamically measured via a catheter placed in portal vein. The indexes of hepatic hemodynamics, including maximal and mean velocity of portal vein flow (PFV(max), PFV(mean)), maximal and minimal velocity of hepatic artery flow (HAV(max), HAV(min)) were measured using colour sonography at baseline, 72 h after infusion octreotide and 7 days after cessation of the infusion.

RESULTS: The portal pressure declined 15.4% on average either in group A or group B after surgery. Portal pressure was significantly decreased after infusion of octreotide in both group A and B as compared with that at baseline. The mean decrease of portal pressure was 20.6%. The portal pressure showed a sustained decrease in group A, but it returned to baseline in group B after stopping of octreotide infusion. The portal pressure in group A and B was statistically different 24 h after stopping octreotide infusion (24.8 +/- 6.5 vs 29.4 +/- 5.8), 48 h (25.3 +/- 6.7 vs 29.9 +/- 7.0), P < 0.05. However, no differences of portal pressure between group A and B before surgery (41.0 +/- 6.6 vs 38.5 +/- 4.7), baseline (32.8 +/- 4.9 vs 33.6 +/- 6.5) and during octreotide infusion were observed. PFV(max) and PFV(mean) were significantly decreased as compared with baseline either before surgery or octreotide infusion. However, HAV(max) and HAV(min) were significantly increased as compared with baseline and before surgery. No relationship between portal pressure and sonography indexes was observed.

CONCLUSIONS: Both dosages of octreotide infusion 50 microg/h and 25 microg/h can significantly reduce portal pressure, although with 25 microg/h of octreotide is reflects it seen returned to baseline. The dosage 50 microg/h of octreotide infusion may be more rational for prevention rebleeding of varices in cirrhotic portal hypertensive patients.