The Molecules: Abnormal Vasculatures in the Splanchnic and Systemic Circulation in Portal Hypertension"

Iwakiri, Yasuko

doi:10.5772/38545

Cited by 26 publications

(34 citation statements)

References 147 publications

(170 reference statements)

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“…reduced response to vasoconstrictor factors; and 3.) mesenteric neoangiogenesis [8][9][10][11]. The increase in NO, maintained in pre-sinusoidal areas, is due to endothelial nitric oxide synthase activation by pro-inflammatory cytokines released by bacterial translocation and shear stress.…”

Section: Hemodynamic Changes Contributing To Hyperdynamic Syndromementioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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The hyperdynamic syndrome is a late consequence of portal hypertension in cirrhosis. The principal hemodynamic manifestations of the hyperdynamic syndrome are high cardiac output, and increased heart rate and total blood volume, accompanied by reduced total systemic vascular resistance. Pathophysiology involves a complex of humoral and neural mechanisms that can determine hemodynamic changes, and lead to hyperdynamic circulation. In this review we focus our attention on the manifestations of the hyperdynamic syndrome. Some of these are well described and directly related to portal hypertension (varices, ascites, hepatic encephalopathy, and hepatorenal syndrome), while others, such as hepatopulmonary syndrome, portopulmonary hypertension, and cirrhotic cardiomyopathy, are less known as clinical manifestations related to cirrhosis and, therefore, merit further investigation.

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Section: Hemodynamic Changes Contributing To Hyperdynamic Syndromementioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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“…11 Details regarding eNOS regulation in liver cirrhosis can be found elsewhere. 2,12 Second, oxidative stress is increased in cirrhosis. LSECs receive oxidative stress in response to a wide variety of agents, such as bacterial endotoxins, viruses, drugs, and ethanol.…”

Section: Decreased Vasodilatorsmentioning

confidence: 99%

“…In cirrhotic livers, NO production/bioavailability is significantly diminished, which contributes to increased intrahepatic vascular resistance. 2,[9][10][11][12] At least two mechanisms explain the decreased NO production. First, the NO synthesizing enzyme endothelial NO synthase (eNOS) is inhibited by negative regulators (such as caveolin-1), which are up-regulated during cirrhosis; as a result, NO production decreases.…”

Section: Decreased Vasodilatorsmentioning

confidence: 99%

“…Experimental models of portal hypertension with or without cirrhosis have shown that other vasodilator molecules, such as carbon monoxide (CO), prostacyclin (PGIs), endocannabinoids, and endothelium-derived hyperpolarizing factor (EDHF) are also induced. 2,9,12 The identity of EDHF is currently unknown, and the candidates include arachidonic acid metabolites [epoxyeicosatrienoic acid (EET)], potassium ions (K + ), components of gap junctions, or hydrogen peroxide. 2 An increase in portal pressure triggers eNOS activation and subsequent NO overproduction.…”

Section: Arterial Vasodilation In the Splanchnic And Systemic Circulamentioning

confidence: 99%

See 1 more Smart Citation

Pathophysiology of Portal Hypertension

Iwakiri¹,

Groszmann²

2014

Variceal Hemorrhage

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Portal hypertension is a major complication of liver disease, which results from a variety of pathological conditions that increase the resistance to the portal blood flow into the liver. The primary cause of portal hypertension in cirrhosis is an increase in intrahepatic vascular resistance due to massive structural changes associated with fibrosis and increased vascular tone in the hepatic microcirculation. As portal hypertension develops, the formation of collateral vessels and arterial vasodilation progress, which results in increased blood flow to the portal circulation. Eventually the hyperdynamic circulatory syndrome develops, leading to esophageal varices or ascites. This review article will summarize the factors that increase 1) intrahepatic vascular resistance and 2) the blood flow in the splanchnic and systemic circulations in liver cirrhosis. Finally, the future directions of basic/clinical research in portal hypertension will be discussed.

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“…These abnormalities are triggered by some vasodilators, such as nitric oxide (NO), in the splanchnic circulation (5,6). Spontane-ous bacterial peritonitis, infections, hypotension, overdose of diuretics, large-volume paracentesis, worsening liver function, and variceal bleeding are the precipitant factors of HRS.…”

Section: Introductionmentioning

confidence: 99%