This study was designed to investigate the effect of octreotide (Sandostatin®, Sandoz), an analogue of somatostatin, on the hemodynamics and glucagon level in portal hypertension. Sixteen portal hypertensive rabbits produced by partial ligation of the portal vein two weeks earlier received an intravenous infusion of octreotide at a dose of 30 μg/h. After infusion of octreotide, a significant reduction in portal venous pressure from 16.2 ± 3.9 mmHg (mean ± SD) to 13.3 ± 4.3 mmHg at 21 minutes and 12.0 ± 4.5 mmHg 42 minutes was noted. A persistent decrease in portal pressure to 11.0 ± 4.5 mmHg 21 minutes after stopping infusion of octreotide was also observed. Portal venous blood flow was decreased significantly from 60.9 ± 13.1 mL/min to 46.9 ± 15.0 ml/min at 21 minutes and to 45.8 ± 12.8 ml/min at 42 minutes. A slight elevation of portal blood flow to 49.0 ± 14.1 ml/min was noted 21 minutes after cessation of octreotide infusion. Portal venous resistance was slightly elevated during infusion of octreotide (before infusion: 2.2 ± 1.4 dyne.s.cm-5, 21 minutes after infusion: 2.4 ± 1.4 dyne.s.cm-5 and 42 minutes after infusion: 2.3 ± 1.3 dyne·s·cm-5), and decreased (1.9 ± 1.0 dyne·s·cm-5, p < 0.1) with a forward significance after stopping infusion. There were no significant changes in systemic arterial pressure during this experiment. A significant decrease (p < 0.05) in glucagon level from 323 ± 93 pg/dl to 267 ± 62 pg/dl at 21 minutes and to 298 ± 88 pg/dl at 42 minutes in the portal vein was noted during the infusion. Therefore, infusion of octreotide at a rate of 30 μg/h reduces portal venous pressure, portal venous blood flow and glucagon level in the portal vein in portal hypertensive rabbits without a significant influence on mean arterial pressure. The decrease in portal pressure is mainly due to a decrease in portal blood flow, not resistance.
|頁（從 - 到）||668-672|
|期刊||Journal of the Formosan Medical Association|
|出版狀態||Published - 1994 十二月 1|
All Science Journal Classification (ASJC) codes