Lactate generation by liver in hemorrhagic shock
| Autor: | John C. O'Brien, Samuel A. Cucinell, Gordon H. Bryant, Bradford S. Goodwin |
|---|---|
| Rok vydání: | 1981 |
| Předmět: |
medicine.medical_specialty
Partial Pressure Shock Hemorrhagic General Biochemistry Genetics and Molecular Biology pCO2 chemistry.chemical_compound Dogs Internal medicine medicine Animals Lactic Acid Vein Acidosis business.industry Venous blood Carbon Dioxide Hydrogen-Ion Concentration Surgery Oxygen Catheter Kinetics medicine.anatomical_structure chemistry Liver Shock (circulatory) Hemorrhagic shock cardiovascular system Cardiology Lactates medicine.symptom business Indocyanine green |
| Zdroj: | Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.). 168(2) |
| ISSN: | 0037-9727 |
| Popis: | Hemorrhagic shock caused a decreased hepatic vein PO2 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 also returned to normal. However, 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 hepa... |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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