Cyclooxygenase-derived products modulate the increased intrahepatic resistance of cirrhotic rat livers

• DOI: 10.1053/jhep.2003.50004
• Publication Date: 2003-02-05T02:43:33Z
• Authors: Mariona Graupera; Joan-Carles Garcí...; Juan G. Abraldes; Carmen Peralta; Mireia Bragulat; Helena Corominola; Jaume Bosch; Juan Rodés
• Keywords: Liver Cirrhosis; Male; 0301 basic medicine; Arachidonic Acid; Cyclooxygenase 2 Inhibitors; Membrane Proteins; Blood Pressure; 6-Ketoprostaglandin F1 alpha; Dinoprost; Nitric Oxide; Methoxamine; 3. Good health; Isoenzymes; Portal System; 03 medical and health sciences; Cyclooxygenase 2; Prostaglandin-Endoperoxide Synthases; Cyclooxygenase 1; Animals; Cyclooxygenase Inhibitors; Adrenergic alpha-Agonists; Carbon Tetrachloride; Liver Circulation

In cirrhotic livers, increased resistance to portal flow, in part due an exaggerated response vasoconstrictors, is the primary factor pathophysiology of hypertension. Our aim was evaluate intrahepatic circulation rat livers α 1 -adrenergic vasoconstrictor methoxamine and mechanisms involved its regulation. A perfusion pressure dose-response curve performed control preincubated with vehicle, nitric oxide synthase blocker NG -nitro-l-arginine (l-NNA), indomethacin cyclooxygenase (COX) inhibitor, l-NNA + indomethacin, or thromboxane (TX) 2 receptor SQ 29,548. TXA production, COX-1 COX-2 mRNA expression, immunostaining for were evaluated. Cirrhotic exhibited a hyperresponse associated overexpression as well production . The disappeared by COX inhibition but not after NO inhibition. 29,548 also corrected methoxamine. conclusion, COX-derived prostanoids, mainly , play major role regulating