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Lactate generation by liver in hemorrhagic shock


, : Lactate generation by liver in hemorrhagic shock. Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine 168(2): 222-227

Hemorrhagic shock caused a decreased hepatic vein P[partial pressure]O2 and pH. This anoxia and acidosis was associated with an increased hepatic vein lactate greater than the arterial and portal vein lactate. This is a reversal of the normal state in which the liver is a consumer of lactate. The normal lactate relationship readily returned following reinfusion of the blood if the hepatic vein PO2 and pH returned to normal. Following a subsequent hemorrhage and reinfusion, the liver continued to produce lactate and the hepatic vein pH remained acidotic, even though the hepatic vein PO2 returned to the control level. Previous studies had shown that catheterization of the hepatic veins in the dog traumatized the liver and the blood samples from that catheter may be misrepresentative of the true state of hepatic venous blood. A study of the level of lactate, PO2, pH, PCO2 and indocyanine green (ICG) compared blood specimens obtained from individually cannulated hepatic veins to those from a common hepatic venous channel (CHVC). Hepatic blood samples from the 2 sites showed no differences for lactate, pH, PCO2 and ICG in the range studied. The CHVC was more dependable for obtaining specimens during profound shock and gave more valid PO2 levels for the lower O2 tensions below 15 mm Hg.

US$19.90

PMID: 6815659

DOI: 10.3181/00379727-168-41264


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