Prostaglandin and portal hypertension

Guarner, Carlos; Soriano, Germán

doi:10.1016/0952-3278(93)90086-c

Cited by 14 publications

(5 citation statements)

References 52 publications

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“…Hence, there is a specific increase in adrenoceptor-linked PGI2 synthesis in portal hypertensive animals, which may contribute to arterial vasodilation in this experimental PVL model. Agonist-stimulated PGI2 production, in general, may be enhanced because several studies have demonstrated that vasopressor-induced changes in splanchnic blood flow in portal hypertensives and cirrhotics are enhanced after inhibition of COX activity with indomethacin [97][98][99][100][101]. Furthermore, evidence for a role of agonist-induced PGI2 release in PHT also is derived from studies on the beneficial effects of long-term TNF-␣ inhibition on systemic hemodynamics in PHT.…”

Section: Cyclooxygenase-dependent Aa Metabolitesmentioning

confidence: 95%

Arachidonic acid metabolites and endothelial dysfunction of portal hypertension

Sacerdoti

Paterini

Pascoli

et al. 2015

Prostaglandins & Other Lipid Mediators

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Increased resistance to portal flow and increased portal inflow due to mesenteric\ud vasodilatation represent the main factors causing portal hypertension in\ud cirrhosis. Endothelial cell dysfunction, defined as an imbalance between the\ud synthesis, release, and effect of endothelial mediators of vascular tone,\ud inflammation, thrombosis, and angiogenesis, plays a major role in the increase of\ud resistance in portal circulation, in the decrease in the mesenteric one, in the\ud development of collateral circulation. Reduced response to vasodilators in liver \ud sinusoids and increased response in the mesenteric arterioles, and, viceversa,\ud increased response to vasoconstrictors in the portal-sinusoidal circulation and\ud decreased response in the mesenteric arterioles are also relevant to the\ud pathophysiology of portal hypertension. Arachidonic acid (AA) metabolites through\ud the three pathways, cyclooxygenase (COX), lipoxygenase, and cytochrome P450\ud monooxygenase and epoxygenase, are involved in endothelial dysfunction of portal \ud hypertension. Increased thromboxane-A2 production by liver sinusoidal endothelial\ud cells (LSECs) via increased COX-1 activity/expression, increased leukotriens,\ud increased epoxyeicosatrienoic acids (EETs) (dilators of the peripheral arterial\ud circulation, but vasoconstrictors of the portal-sinusoidal circulation),\ud represent a major component in the increased portal resistance, in the decreased \ud portal response to vasodilators and in the hyper-response to vasoconstrictors.\ud Increased prostacyclin (PGI2) via COX-1 and COX-2 overexpression, and increased\ud EETs/heme-oxygenase-1/K channels/gap junctions (endothelial derived\ud hyperpolarizing factor system) play a major role in mesenteric vasodilatation,\ud hyporeactivity to vasoconstrictors, and hyper-response to vasodilators. EETs,\ud mediators of liver regeneration after hepatectomy and of angiogenesis, may play a\ud role in the development of regenerative nodules and collateral circulation,\ud through stimulation of vascular endothelial growth factor (VEGF) inside the liver\ud and in the portal circulation. Pharmacological manipulation of AA metabolites may\ud be beneficial for cirrhotic portal hypertension

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Section: Cyclooxygenase-dependent Aa Metabolitesmentioning

confidence: 95%

Arachidonic acid metabolites and endothelial dysfunction of portal hypertension

Sacerdoti

Paterini

Pascoli

et al. 2015

Prostaglandins & Other Lipid Mediators

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“…This circulatory change is caused by a variety of vasoactive factors, such as cytokines, prostacyclins, and nitric oxide [14][15][16][17][18] . Infection or bleeding, which are frequent complications in cirrhotic patients, increase the nitric oxide production and result in aggravation of the hyperdynamic circulation [19] .…”

Section: Introductionmentioning

confidence: 99%

Effect of Prometheus liver assist system on systemic hemodynamics in patients with cirrhosis: A randomized controlled study

Dethloff¹,

Tofteng²,

Frederiksen³

et al. 2008

WJG

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“…The activation of contractile elements in the fat-storing cells may play a particular role. These cells are controlled by numerous regulatory systems, including those for glucagon, nitric ox-ide, endothelin, cytokines and prostaglandins (11,(38)(39)(40)(41)(42). It is important to note that recent experiments have indicated that splanchnic and hepatic nitric oxide synthase activity is decreased in experimental cirrhosis, and that transfection of the nitric oxide synthase gene reduces portal pressure substantially (43,44).…”

Section: Hepatosplanchnic Circulation In Cirrhosismentioning

confidence: 99%

Splanchnic and Systemic Haemodynamic Derangement in Decompensated Cirrhosis

Möller

Bendtsen

Henriksen

2001

Canadian Journal of Gastroenterology

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Patients with cirrhosis and portal hypertension exhibit characteristic hemodynamic changes with hyperkinetic systemic circulation, abnormal distribution of blood volume and neurohumoral dysregulation. Their plasma and noncentral blood volumes are increased. Splanchnic vasodilation is of pathogenic significance to the low systemic vascular resistance and abnormal volume distribution of blood, which are important elements in the development of the concomitant cardiac dysfunction, recently termed 'cirrhotic cardiomyopathy'. Systolic and diastolic functions are impaired with direct relation to the degree of liver dysfunction. Significant pathophysiological mechanisms are reduced beta-adrenergic receptor signal transduction, defective cardiac excitation-contraction coupling and conductance abnormalities. Vasodilators such as nitric oxide and calcitonin gene-related peptide are among the candidates in vasodilation and increased arterial compliance. Reflex-induced, enhanced sympathetic nervous system activity, activation of the renin-angiotensin aldosterone system, and elevated circulation vasopressin and endothelin-1 are implicated in hemodynamic counter-regulation in cirrhosis. Recent research has focused on the assertion that the hemodynamic and neurohumoral abnormalities in cirrhosis are part of a general cardiovascular dysfunction, influencing the course of the disease with the reduction of organ function, with sodium and water retention as the outcome. These aspects are relevant to therapy.

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Prostaglandin and portal hypertension

Cited by 14 publications

References 52 publications

Arachidonic acid metabolites and endothelial dysfunction of portal hypertension

Arachidonic acid metabolites and endothelial dysfunction of portal hypertension

Effect of Prometheus liver assist system on systemic hemodynamics in patients with cirrhosis: A randomized controlled study

Splanchnic and Systemic Haemodynamic Derangement in Decompensated Cirrhosis

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