ET-1-Induced Portal Hypertension in Rats and Hepatic Sinusoid Endothelium Changes Intervened by Salvianolic-acid B
Hongwei Wang
Abstract
Hongwei Wang
Abstract
Objective: To study the morphologic change of hepatic sinusoid endothelium during ET-1 induced portal hypertension in rats and its intervention by Salvianolic-acid B. Methods: Twenty SD rats were randomly divided into four groups,then in situ liver perfusion was performed to detect the portal pressure of rats. We performed an in situ perfusion of rat livers with 10-9 mol/L ET-1 and 10-5 mol/L Salvianolic-acid B; after 5-minute perfusion,morphologic methods were used to study the changes of hepatic sinusoid endothelium during ET-1 induced portal hypertension and intervention by Salvianolic-acid B. Results: Intraportal infusion of 10-9 mol/L endothelin-1 significantly elevated portal venous pressure. The reduction in the number of fenestrae of sinusoidal endothelial cells was obvious during ET-1 induced portal hypertension; SA-B significantly down-regulated the high portal vein pressure induced by extragenous ET-1,the number of fenestrae of sinusoidal endothelial cells was much more than in control group. Conclusion: Hepatic sinusoid endothelium change is the vital cause of portal hypertension induced by ET-1.
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Objective: To study the morphologic change of hepatic sinusoid endothelium during ET-1 induced portal hypertension in rats and its intervention by Salvianolic-acid B. Methods: Twenty SD rats were randomly divided into four groups,then in situ liver perfusion was performed to detect the portal pressure of rats. We performed an in situ perfusion of rat livers with 10-9 mol/L ET-1 and 10-5 mol/L Salvianolic-acid B; after 5-minute perfusion,morphologic methods were used to study the changes of hepatic sinusoid endothelium during ET-1 induced portal hypertension and intervention by Salvianolic-acid B. Results: Intraportal infusion of 10-9 mol/L endothelin-1 significantly elevated portal venous pressure. The reduction in the number of fenestrae of sinusoidal endothelial cells was obvious during ET-1 induced portal hypertension; SA-B significantly down-regulated the high portal vein pressure induced by extragenous ET-1,the number of fenestrae of sinusoidal endothelial cells was much more than in control group. Conclusion: Hepatic sinusoid endothelium change is the vital cause of portal hypertension induced by ET-1.
Key concepts: Sinusoid, Portal hypertension, Perfusion, Endothelium, Medicine, Portal venous pressure, Internal medicine, Endocrinology