Role of endothelium in the abnormal response of mesenteric vessels in rats with portal hypertension and liver cirrhosis
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Cited by (75)
Prostacyclin decreases splanchnic vascular contractility in cirrhotic rats
2014, Hepatobiliary and Pancreatic Diseases InternationalPortal Hypertension and Gastrointestinal Bleeding
2010, Sleisenger and Fordtran’s Gastrointestinal and Liver Disease- 2 Volume Set: Pathophysiology, Diagnosis, Management, Expert Consult Premium Edition - Enhanced Online Features and PrintPortal Hypertension and Variceal Hemorrhage
2008, Medical Clinics of North AmericaCitation Excerpt :Cirrhosis is associated with a hyperdynamic circulatory state that is characterized by peripheral and splanchnic vasodilation, reduced mean arterial pressure, and increased cardiac output. NO-mediated splanchnic vasodilatation [8–16] produces an increase in inflow of systemic blood into the portal circulation, which causes an increase in portal pressure [17]. Portal pressure is most commonly determined by the hepatic vein pressure gradient (HVPG), which is the difference between the wedged hepatic venous pressure (reflecting the hepatic sinusoidal pressure) and free hepatic vein pressure [18,19].
Vasoactive factors and hemodynamic mechanisms in the pathophysiology of portal hypertension in cirrhosis
2008, Molecular Aspects of MedicineNitric oxide and portal hypertension: Interface of vasoreactivity and angiogenesis
2006, Journal of HepatologyCitation Excerpt :In contrast to diminished intrahepatic bioavailability of NO, the splanchnic (and systemic) circulation experiences a relative excess in regional NO generation [7]. This increased production is largely endothelium and eNOS dependent [35–37]. However, iNOS and nNOS have been implicated as well and studies in NOS isoform gene deletion mice have not fully clarified the matter [38–41].
Reduced capacitative calcium entry in the mesenteric vascular bed of bile duct-ligated rats
2005, European Journal of Pharmacology