Z Y Wu1, X J Zhao1, Z Jiao1, Z P Chen1, Y L Kuang1. 1. Zhi-Yong Wu, Xiao-Jie Zhao, Zhe Jiao, Zhi-Ping Chen, Yao-Ling Kuang, Department of Surgery, Renji Hospital Shanghai Second Medical University, Shanghai 200001, China.
Abstract
AIM: To investigate the effects of somatostatin analog on splanchnic hemodynamics and plasma glucagon level in portal hypertensive rats. METHODS: Twenty-eight male Sprague-Dawley rats were equally divided into a intrahepatic portal hypertension (IHPH) model group (n = 14, established by injection of CCl4) and a prehepatic portal hypertension (PHPH) model group (n = 14, established by stenosis of the portal vein). Animals in each group were subdivided into an octreotide treatment (injection) group and a control (normal saline injection) group. Seven age-matched unmodeled/untreated normal rats served as controls. The mean systemic arterial pressure (MSAP) and free portal venous pressure (FPP) were measured. The splanchnic blood flow was detected by injection of toad blood red cell labelled with (51)Cr and (125)I·T3. The concentration of plasma glucagon was determined by radioimmunoassay. RESULTS: All rats with portal hypertension showed significantly decreased splanchnic blood flow and FPP in response to octreotide treatment, as well as markedly increased splanchnic vascular and portal venous resistance. The octreotide treatment did not appear to significantly lower the plasma glucagon levels in either the peripheral or the portal veins. CONCLUSION: Octreotide induces a decrease in splanchnic blood flow in rats with portal hypertension, and this effect results primarily from direct vasoconstriction and to a lesser extent from decreased plasma glucagon level.
AIM: To investigate the effects of somatostatin analog on splanchnic hemodynamics and plasma glucagon level in portal hypertensiverats. METHODS: Twenty-eight male Sprague-Dawley rats were equally divided into a intrahepatic portal hypertension (IHPH) model group (n = 14, established by injection of CCl4) and a prehepatic portal hypertension (PHPH) model group (n = 14, established by stenosis of the portal vein). Animals in each group were subdivided into an octreotide treatment (injection) group and a control (normal saline injection) group. Seven age-matched unmodeled/untreated normal rats served as controls. The mean systemic arterial pressure (MSAP) and free portal venous pressure (FPP) were measured. The splanchnic blood flow was detected by injection of toad blood red cell labelled with (51)Cr and (125)I·T3. The concentration of plasma glucagon was determined by radioimmunoassay. RESULTS: All rats with portal hypertension showed significantly decreased splanchnic blood flow and FPP in response to octreotide treatment, as well as markedly increased splanchnic vascular and portal venous resistance. The octreotide treatment did not appear to significantly lower the plasma glucagon levels in either the peripheral or the portal veins. CONCLUSION:Octreotide induces a decrease in splanchnic blood flow in rats with portal hypertension, and this effect results primarily from direct vasoconstriction and to a lesser extent from decreased plasma glucagon level.