摘要
In the present study we observed dynamically and systemically the changes of plasma somatostatin and glucagon in the peripheral and portal vein, and the changes of pancreatic immunopathology in the course of development of cirrhosis induced by CCl<sub>4</sub> and after portacaval shunt （PCS） in the cirrhotic rats as well as investigated their causes and correlationship. The results showed that hyperglucagonemia was caused by spontaneous portosystemic shunting and surgically induced portacaval anastomosis. Moreover, there was much higher level of glucagon in the portal vein with corresponding increase of A cells in PCS rats than those in the controls, indicating that another cause for elevation of glucagon was hypersecretion of pancreatic A cells. Our data demonstrated that both deterioration of liver function and portosystemic shunting might not be responsible for the elevated level of somatostatin in the cirrhotic rats with PCS. However, there was a closed positive correlation between plasma glucagon and somatostatin. Thus it was concluded that hyperglucagonemia stimulated the release of somatostatin. In view of the fact the elevated level of glucagon was much higher than that of somatostatin, there was probably a relative lack of somatostatin in cirrhosis with portal hypertension.
In the present study we observed dynamically and systemically the changes of plasma somatostatin and glucagon in the peripheral and portal vein, and the changes of pancreatic immunopathology in the course of development of cirrhosis induced by CCl_4 and after portacaval shunt (PCS) in the cirrhotic rats as well as investigated their causes and correlationship. The results showed that hyperglucagonemia was caused by spontaneous portosystemic shunting and surgically induced portacaval anastomosis. Moreover, there was much higher level of glucagon in the portal vein with corresponding increase of A cells in PCS rats than those in the controls, indicating that another cause for elevation of glucagon was hypersecretion of pancreatic A cells. Our data demonstrated that both deterioration of liver function and portosystemic shunting might not be responsible for the elevated level of somatostatin in the cirrhotic rats with PCS. However, there was a closed positive correlation between plasma glucagon and somatostatin. Thus it was concluded that hyperglucagonemia stimulated the release of somatostatin. In view of the fact the elevated level of glucagon was much higher than that of somatostatin, there was probably a relative lack of somatostatin in cirrhosis with portal hypertension.
