Systemic and hepatic hemodynamic changes in acute liver injury.
Systemic and hepatic circulatory changes were studied in rats over the course of acute liver injury. Hepatic injury was induced by intraperitoneal injection of D-galactosamine (1.1 g/kg), and systemic and hepatic hemodynamics were measured over a 72-h period using a radioactive microsphere technique with direct measurement of arterial, portal venous, and hepatic venous blood oxygen content. Cardiac output increased to a maximum at 48 h, producing a marked increase (450%) in hepatic arterial blood flow so that it became the dominant supply of oxygen at the time of maximal hepatic injury. A subsequent increase in portal venous flow resulted in an overall increase in total hepatic blood flow of 500%. At this point the oxygen delivery by the hepatic arterial and portal venous systems was equal. These circulatory changes returned to control values by 72 h with recovery of liver function. These results demonstrate the development of a hyperdynamic circulation and a marked change in the normal relationship between portal venous and hepatic arterial blood flows that occur during hepatic injury.
Makin
A J
AJ
Institute of Liver Studies, King's College School of Medicine and Dentistry, London, UK.
Hughes
R D
RD
Williams
R
R
D000208:Acute Disease; D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D002302:Cardiac Output; D005688:Galactosamine / Q000633:toxicity; D005690:Galactose / Q000378:metabolism; D006439:Hemodynamics; D006499:Hepatic Artery; D008099:Liver / Q000098:blood supply / Q000293:injuries* / Q000378:metabolism; D008102:Liver Circulation; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D011169:Portal Vein; D051381:Rats; D017208:Rats, Wistar; D013152:Splanchnic Circulation; D013997:Time Factors; D014655:Vascular Resistance
D005688:Galactosamine; D010100:Oxygen; D005690:Galactose