Bile Salts, Bile Flow, and Cholestasis

Quiroga, Jorge

doi:10.1007/978-3-642-76802-6_8

Cited by 1 publication

(1 citation statement)

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“…However, in some models, acute reversible cholestasis occurs after LPS injection. The pathogenesis of this form of cholestasis, which is clinically represented by the cholestasis associated with sepsis, severe infection or acute severe inflammatory disease, is unknown (Quiroga, 1992). It has been attributed, at least in part, to an excessive production of cysteinyl-LTs (Keppler et al, 1988), since the injection of high doses of LTC 4 to the guinea pig induces cholestasis, which also develops after the simultaneous administration of pharmacological doses of both, LTD4 and PGE 2, to the rat (Keppler et al, 1985).…”

Section: Endotoxin-induced Liver Injurymentioning

confidence: 99%

Liver cytoprotection by prostaglandins

Quiroga

Prìeto

1993

Pharmacology & Therapeutics

115

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During the last decade intensive work on the relationships between the liver and the arachidonic acid cascade has greatly expanded our knowledge of this area of research. The liver has emerged as the major organ participating in the degradation and elimination of arachidonate products of systemic origin. The synthesis in the liver of arachidonate products derived from the cyclooxygenase, lipoxygenase and cytochrome P450 system pathways has been demonstrated. The participation of leukotriene B4 and cysteinyl-leukotrienes as mediators of liver damage and the possible therapeutic usefulness of prostaglandins (PGs) in acute liver injury has attracted the interest of clinicians. This article reviews the essential features regarding the role of arachidonate metabolites in liver disease and specially focuses on the cytoprotective effects on the liver displayed by PGE2, PGE1, PGI2 and synthetic PG analogs in experimental models of liver damage induced by ischemia-reperfusion injury, carbon tetrachloride, bacterial lipopolysaccharide and viral hepatitis and on the possible mechanisms underlying liver cytoprotection in these experimental models. The therapeutic usefulness of PGs in clinical practice is critically analyzed on the basis of available evidence in patients with fulminant hepatic failure and primary graft nonfunction following liver transplantation.

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Section: Endotoxin-induced Liver Injurymentioning

confidence: 99%