Current concepts on the role of nitric oxide in portal hypertension
| Autor: | Jacob George, Liang Shuo Hu, Jianhua Wang |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
Liver Cirrhosis
medicine.medical_specialty Cirrhosis Portal venous pressure Vasodilation Review Nitric Oxide Internal medicine Hypertension Portal Medicine Animals Humans Nitric Oxide Donors Splanchnic Circulation Antihypertensive Agents business.industry Portal Vein Gastroenterology General Medicine medicine.disease Collateral circulation Portal Pressure Endocrinology medicine.anatomical_structure Vascular resistance Cardiology Portal hypertension Nitric Oxide Synthase business Splanchnic Signal Transduction |
| Zdroj: | World journal of gastroenterology. 19(11) |
| ISSN: | 2219-2840 |
| Popis: | Portal hypertension (PHT) is defined as a pathological increase in portal venous pressure and frequently accompanies cirrhosis. Portal pressure can be increased by a rise in portal blood flow, an increase in vascular resistance, or the combination. In cirrhosis, the primary factor leading to PHT is an increase in intra-hepatic resistance to blood flow. Although much of this increase is a mechanical consequence of architectural disturbances, there is a dynamic and reversible component that represents up to a third of the increased vascular resistance in cirrhosis. Many vasoactive substances contribute to the development of PHT. Among these, nitric oxide (NO) is the key mediator that paradoxically regulates the sinusoidal (intra-hepatic) and systemic/splanchnic circulations. NO deficiency in the liver leads to increased intra-hepatic resistance while increased NO in the circulation contributes to the hyperdynamic systemic/splanchnic circulation. NO mediated-angiogenesis also plays a role in splanchnic vasodilation and collateral circulation formation. NO donors reduce PHT in animals models but the key clinical challenge is the development of an NO donor or drug delivery system that selectively targets the liver. |
| Databáze: | OpenAIRE |
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