| DYNAMIC OBSERVATION ON THE CHANGES OF PLASMA SOMATOSTATIN AND GLUCAGON DURING THE DEVELOPMENT OF CIRRHOSIS AND AFTER PORTACAVAL SHUNTING IN THE CIRRHOTIC RATS |
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| 引用本文： | 吴志勇,黄安,郑忠华,陈聿修,陈治平,邝耀麟,小野慶一,金充. DYNAMIC OBSERVATION ON THE CHANGES OF PLASMA SOMATOSTATIN AND GLUCAGON DURING THE DEVELOPMENT OF CIRRHOSIS AND AFTER PORTACAVAL SHUNTING IN THE CIRRHOTIC RATS[J]. 上海第二医科大学学报, 1992, 0(1) |
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| 作者姓名： | 吴志勇 黄安 郑忠华 陈聿修 陈治平 邝耀麟 小野慶一 金充 |
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| 作者单位： | Department of Surgery，Renji Hospital，SSMU，Shanghai，Department of Surgery，Renji Hospital，SSMU，Shanghai，Department of Surgery，Renji Hospital，SSMU，Shanghai，Department of Surgery，Renji Hospital，SSMU，Shanghai，Department of Surgery，Renji Hospital，SSMU，Shanghai，Department of Surgery，Renji Hospital，SSMU，Shanghai，Department of Surgery，Hirosaki University School of Medicine，Hirosaki，Japan，Department of Surgery，Hirosaki University School of Medicine，Hirosaki，Japan |
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| 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_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.
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DYNAMIC OBSERVATION ON THE CHANGES OF PLASMA SOMATOSTATIN AND GLUCAGON DURING THE DEVELOPMENT OF CIRRHOSIS AND AFTER PORTACAVAL SHUNTING IN THE CIRRHOTIC RATS |
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| Wu Zhiyong Huang An Zheng Zhonghua Chen Yuxiu Chen Zhiping Kuang Yaolin. DYNAMIC OBSERVATION ON THE CHANGES OF PLASMA SOMATOSTATIN AND GLUCAGON DURING THE DEVELOPMENT OF CIRRHOSIS AND AFTER PORTACAVAL SHUNTING IN THE CIRRHOTIC RATS[J]. Journal of Shanghai Second Medical University(Foreign Language Edition), 1992, 0(1) |
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| Authors: | Wu Zhiyong Huang An Zheng Zhonghua Chen Yuxiu Chen Zhiping Kuang Yaolin |
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| Affiliation: | Wu Zhiyong Huang An Zheng Zhonghua Chen Yuxiu Chen Zhiping Kuang Yaolin Department of Surgery,Renji Hospital,SSMU,Shanghai Keiichi Ono Mitsuru Konn Department of Surgery,Hirosaki University School of Medicine,Hirosaki,Japan |
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| Abstract: | 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. |
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| Keywords: | somatostatin glucagon pancreatic immunopathology cirrhosis of liver portal hypertension portacaval shunt deterioration of liver function |
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