Hepatic oxygen supply and plasma lactate and glucose in endotoxic shock.
Hepatic oxygen supply and selected blood parameters were recorded in fasted male rates given 20--30 mg/kg Escherichia coli endotoxin intraperitoneally. Mortality was 70% within 24 hours. Measurements during the initial eight hours postendotoxin recorded no differences of hematocrit, systemic arterial pressure, or arterial pO2 between survivors and eventual nonsurvivors. However, by the sixth or eighth hour nonsurvivors showed significantly higher plasma lactate, lower plasma glucose and blood pH, and a greater degree of hypocapnea. In addition, a mean hepatic pO2 had decreased from 25.2 mm Hg during the control to 3.8 mm Hg after six hours. A decline of hepatic oxygen supply also occurred in surviving rats but was significantly less severe. Control rats showed a mild degree of respiratory alkalosis but were otherwise stable over eight hours. The relationship of hepatic oxygen supply to differences of plasma lactate and glucose is discussed. Failure of hepatic circulation is cited as the probable cause of extensive liver anoxia and related developments in nonsurviving endotoxic rats.
D000136:Acid-Base Equilibrium; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D004926:Escherichia coli; D007773:Lactates / Q000097:blood*; D008099:Liver / Q000032:analysis*; D008297:Male; D010100:Oxygen / Q000032:analysis*; D051381:Rats; D012772:Shock, Septic / Q000097:blood / Q000378:metabolism*
D001786:Blood Glucose; D007773:Lactates; D002245:Carbon Dioxide; D010100:Oxygen