Hepatocyte dysfunction in thermal injury.
Transmembrane potential difference (PD) is a reliable indicator of cellular function. Decreased PD in hepatocytes in hemorrhagic shock occurred concomitant with decreased adenosine triphosphate (ATP), suggesting energy depletion as the mechanism of cell dysfunction. This study correlates changes in liver and muscle PD with hepatocyte ATP, glucose-6-phosphate (G-6-P), and lactate levels in burn shock and resuscitation. Six adult female baboons were subjected to 52.4 +/- 6.3% body surface area third-degree scald burns. The animals were resuscitated using the Parkland formula, after the muscle PD had fallen to -70 mV. Liver PD decreased from 46.2 +/- 2.4 mV to 22.4 +/- 3.8 mV in burn shock. The PD recovered toward normal with resuscitation. ATP and G-6-P contents did not change significantly, while lactate rose threefold in burn shock. A severe cellular derangement was indicated by this marked hepatocyte depolarization. Maintenance of normal intracellular ATP excludes energy depletion as the mechanism of this cell dysfunction. These findings are consistent with failure of active ion transport or changes in cell membrane permeability which were partially recovered during fluid resuscitation.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002056:Burns / Q000503:physiopathology*; D002462:Cell Membrane / Q000503:physiopathology; D005260:Female; D006439:Hemodynamics; D008099:Liver / Q000166:cytology* / Q000503:physiopathology; D008564:Membrane Potentials; D010215:Papio; D012151:Resuscitation; D012769:Shock / Q000503:physiopathology; D014563:Urodynamics
D000255:Adenosine Triphosphate