Cellular function in liver and muscle during hemorrhagic shock in primates.
The results of this study demonstrated that muscle ATP levels were sustained in hemorrhagic shock despite marked deterioration of muscle function as indicated by a decline in PD. This indicated that energy depletion was not the primary basis of the cellular dysfunction in hemorrhagic shock. Cellular dysfunction and metabolic abnormalities in the liver occurred earlier during the course of hemorrhagic shock than in muscle. Other studies were cited in which it was suggested that inhibition of the membrane bound sodium and potassium active transport mechanism is the likely cause of tissue electrolyte and fluid shifts observed during prolonged periods of hemorrhagic shock.
D000255:Adenosine Triphosphate / Q000097:blood / Q000378:metabolism; D000818:Animals; D005260:Female; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D007773:Lactates / Q000097:blood; D008099:Liver / Q000503:physiopathology*; D008102:Liver Circulation; D008564:Membrane Potentials; D009132:Muscles / Q000098:blood supply / Q000503:physiopathology*; D010215:Papio; D010725:Phosphocreatine / Q000378:metabolism; D011323:Primates; D012769:Shock / Q000150:complications* / Q000503:physiopathology; D012771:Shock, Hemorrhagic / Q000209:etiology / Q000503:physiopathology*
D007773:Lactates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate