Evidence for additional mediator in prostaglandin-induced choleresis

PGA1 and PGF2alpha were administered to isolated perfused porcine and canine livers to determine whether these hormones could induce hepatic choleresis. PGA1 (25 microgram/kg/10 min) decreased portal venous resistance, but had no effect on bile flow, oxygen, pyruvate, or lactate consumption in canine livers. PGF2alpha increased portal venous resistance and weight gain while decreasing bile flow and oxygen consumption in canine livers. At high doses (50 microgram/kg/10 min) these effects resulted in irreversible outflow block. At low doses (5 microgram/kg/10 min) these trends were reversible. Porcine livers did not exhibit the outflow block syndrome after PGF2alpha administration (100 microgram/kg/10 min); however, choleresis was not observed. Thus, the in-vivo choleretic effects of prostaglandins previously reported are probably mediated partially or wholly by extrahepatic release of other hormones, neurological stimulation or alterations in mesenteric blood flow.