RESUMO
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.
RESUMO
The splanchnic and systemic hemodynamics were measured by radioactive microsphere techniques in a PVL rat's model with portal hypertension. The portal-hypertensive rats (1.75 +/- 0.24 vs. 1.23 +/- 0.13 kPa, P < 0.001) with greater than 93% portal-systemic shunting had an increase in portal venous inflow by 50% (8.97 +/- 0.8 vs. 6.03 +/- 0.28 ml.min-1.100gBW-1; P < 0.001) and a concomitant decrease by 40% in splanchnic arteriolar resistance (0.27 +/- 0.05 vs. 0.42 +/- 0.05kPa.ml-1.min-1.100gBW-1; P < 0.01) compared with control rats. Cardiac index (54.6 +/- 4.4 vs. 36.5 +/- 3.0 ml.min-1.100gBW-1) was elevated by 50% (P < 0.001), and total peripheral resistance (0.052 +/- 0.006 vs. 0.084 +/- 0.009 kPa.ml-1.min-1.100gBW-1) was decreased by 40% (P < 0.001). The resistance to portal blood flow in portal vein-stenotic rats (0.087 +/- 0.011kPa.ml-1.min-1) was similar to that in control rats (0.076 +/- 0.01kPa.ml-1.min-1), indicating that the hyperdynamic portal venous inflow, not resistance, was the mainstay of the elevated portal venous pressure. Which is in favor of the forward flow theory of portal hypertension. The systemic hemodynamic parameters were secondary to the splanchnic hemodynamic changes.
Assuntos
Hipertensão Portal/fisiopatologia , Circulação Esplâncnica , Animais , Hemodinâmica , Ligadura , Masculino , Veia Porta , Ratos , Ratos Sprague-DawleyRESUMO
Carbon tetrachloride was used to induce cirrhosis in 81 Wistar rats. The animals were divided into three groups to receive end-to-side mesocaval shunt (MCS), end-to-side portacaval shunt (PCS) and Sham operation as control, respectively. Dynamic values of blood glucose and hormones for regulating glucose metabolism, SGPT, serum glycine conjugated cholic acid (CCA) and free serum amino acids were determined and compared with those obtained from 10 normal rats. The determinations suggested that the insulin level depended on the severity of hepatocellular damage with hyperglucagonemia after portasystemic shunt, and CCA was markedly elevated in MCS rats after interruption of the enterohepatic circulation. Changes of CCA were also influenced by hyperglucagonemia and poor liver function in PCS rats. Increase in the aromatic amino acids (AAA) level was related to the impaired hepatic function and hyperglucagonemia. However, decrease in the branched-chain amino acids (BCAA) level was not likely in response to the serum insulin level. Therefore, it is concluded that imbalance of serum amino acids has partial relationship with the derangement of glucose metabolic hormones.