vein-stenosed rats without affecting the degree of mes-The hemodynamic effects of long-term administration enteric-systemic shunts. (HEPATOLOGY 1996;23:537-543.) of octreotide in portal hypertension has not been established. In addition, whether long-term octreotide treatment prevents the development of portosystemic shunts
Octreotide is a synthetic long-acting analog of sohas not yet been evaluated. Hence, the current study matostatin. 1 This drug has been shown to have potenwas undertaken to evaluate the effects of long-term adtial beneficial effects in the management of acute hemministration of octreotide in rats with portal vein stenoorrhage from esophageal varices. [2][3][4] Hemodynamic sis. Immediately after portal vein stenosis or sham operstudies in portal hypertensive animals showed that ation, rats were given either a long-term octreotide acute intravenous infusion of octreotide resulted in a administration of 100 mg/kg or a placebo every 12 hours dose-dependent decrease in portal pressure associated by subcutaneous injection for 14 consecutive days. Systemic hemodynamics and regional blood flows, degree with increases in vascular resistances, indicating vasoof mesenteric-systemic shunts, and plasma glucagon constrictive effects of octreotide. 5 In addition, in portal concentrations were measured after the final dose of vein-stenosed rats, a 4-day course of octreotide treatoctreotide or placebo. A fifth group of portal vein-stement starting at the time of portal vein stenosis amelionosed rats received hemodynamic and plasma glucagon rated vasodilatation and sodium retention. 6 However, measurements after 1-day octreotide treatment given at in cirrhotic patients, short-term administration of oc-14 days after surgery. Long-term octreotide treatment treotide markedly decreased hepatic and azygous blood modified the hyperdynamic circulation without affectflows with minimal effect on portal pressure, and the ing the degree of mesenteric-systemic shunts, and 1-day systemic hemodynamic values, including cardiac outoctreotide treatment decreased portal tributary blood put, mean arterial pressure, and systemic vascular reflow without affecting the portal pressure, systemic hemodynamics, and degree of mesenteric-systemic shunts. sistance, were not affected. [7][8][9][10][11] The mechanism of action Plasma glucagon levels were decreased in portal veinof octreotide in portal hypertension has not been docustenosed rats receiving either long-term or 1-day octreomented. No systemic and regional hemodynamic data tide compared with rats receiving placebo. In contrast, have yet been reported after long-term administration chronic octreotide treatment did not affect any of the of octreotide in portal hypertensive animals. Moreover, hemodynamic values or plasma glucagon levels in shamwhether chronic octreotide treatment prevents the deoperated rats. In conclusion, long-term administration velopment of portosystemic shunts, as shown by other of octreotide modified in part the development of portal vasoactive drugs such as propranolol, clonidine, or nihypertension and hyperdynamic circulation in portal tric oxide synthase inhibitor, has not yet been evaluated. [12][13][14][15] Therefore, the current study was undertaken Abbreviations: CI, cardiac index; SVR, systemic vascular resistance; MAP, to evaluate the effect of long-term octreotide treatment mean arterial pressure; RVR, renal vascular resistance. on hemodynamic changes, degree of portosystemic From the