Roles of hemodynamic alterations in portal hypertension and cirrhosis
Portal hypertension (PHT) is the most common cause of cirrhosis. Since portal pressure is dependent upon intrahepatic resistance and splanchnic blood flow, hemodynamic changes in intrahepatic, systemic, and portosystemic collateral circulation can contribute to or be affected by its perturbation. In...
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| Format: | Article |
| Language: | zho |
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Editorial Department of Journal of Clinical Hepatology
2013-04-01
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| Series: | Linchuang Gandanbing Zazhi |
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| Online Access: | http://www.lcgdbzz.org/qk_content.asp?id=5311&ClassID=31291455 |
| Summary: | Portal hypertension (PHT) is the most common cause of cirrhosis. Since portal pressure is dependent upon intrahepatic resistance and splanchnic blood flow, hemodynamic changes in intrahepatic, systemic, and portosystemic collateral circulation can contribute to or be affected by its perturbation. Intrahepatic vascular regulation and development of intrahepatic resistance involve multiple cellular and molecular mechanisms, such as hepatic stellate cells and sinusoidal endothelial cells and nitric oxide (NO) signaling, especially through the endothelial nitric oxide synthase (eNOS). Studies have implicated increased intrahepatic resistance and hyperdynamic circulatory alterations with expansion of collateral circulation as playing central roles in the pathogenesis of PHT. A detailed understanding of these processes in PHT is critical to developing effective treatment options and reducing the currently high rates of morbidities and mortality related to hemodynamic alterations in patients with cirrhosis. In this review, the roles of PHT-related vascular remodeling on severity and complications (including cardiac, kidney, and pulmonary) of cirrhosis, and of collateral circulation angiogenesis are discussed, as they represent potential targets for treatment of portal hypertension. |
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| ISSN: | 1001-5256 1001-5256 |