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Cirrhotic portal hypertension: From pathophysiology to novel therapeutics

World Journal of Gastroenterology 2020年第40期26卷 6111-6140页

作者： Lakmie S Gunarathne Harinda Rajapaksha Nicholas Shackel Peter W Angus Chandana B Herath Department of Medicine Melbourne Medical SchoolThe University of MelbourneHeidelbergVIC 3084Australia School of Molecular Science College of ScienceHealth and EngineeringLa Trobe UniversityBundooraVIC 3086Australia ANZAC Research Institute ConcordNSW 2139Australia Department of Gastroenterology Austin HealthHeidelbergVIC 3084Australia South Western Sydney Clinical School Faculty of MedicineUniversity of New South WalesIngham Institute for Applied Medical Research1 Campbell StreetLiverpoolNSW 2170Australia

Portal hypertension and bleeding from gastroesophageal varices is the major cause of morbidity and mortality in patients with cirrhosis. Portal hypertension is initiated by increased intrahepatic vascular resistance and a hyperdynamic circulatory state. The latter is characterized by a high cardiac output, increased total blood volume and splanchnic vasodilatation, resulting in increased mesenteric blood flow. Pharmacological manipulation of cirrhotic portal hypertension targets both the splanchnic and hepatic vascular beds. Drugs such as angiotensin converting enzyme inhibitors and angiotensin Ⅱ type receptor 1 blockers, which target the components of the classical renin angiotensin system(RAS), are expected to reduce intrahepatic vascular tone by reducing extracellular matrix deposition and vasoactivity of contractile cells and thereby improve portal hypertension. However, these drugs have been shown to produce significant offtarget effects such as systemic hypotension and renal failure. Therefore, the current pharmacological mainstay in clinical practice to prevent variceal bleeding and improving patient survival by reducing portal pressure is non-selective-blockers(NSBBs). These NSBBs work by reducing cardiac output and splanchnic vasodilatation but most patients do not achieve an optimal therapeutic response and a significant proportion of patients are unable to tolerate these *** statins, used alone or in combination with NSBBs, have been shown to improve portal pressure and overall mortality in cirrhotic patients, further randomized clinical trials are warranted involving larger patient populations with clear clinical end points. On the other hand, recent findings from studies that have investigated the potential use of the blockers of the components of the alternate RAS provided compelling evidence that could lead to the development of drugs targeting the splanchnic vascular bed to inhibit splanchnic vasodilatation in portal hypertension. This rev

关键词： Portal hypertension Cirrhosis Intrahepatic vascular resistance Hyperdynamic circulatory state splanchnic vasodilatation Portal blood flow Non-selective betablockers Alternate renin angiotensin system

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