title: Effect of hemorrhagic shock on hepatic transmembrane potentials and intracellular electrolytes, in vivo.
abstract: In this study we investigated in vivo changes in hepatic cellular electrolytes and resting transmembrane potentials (Em) during hemorrhagic shock. Hepatic Na-K transport and cell volume regulation were assessed in vitro. Rats were bled and the ensuing hypotension (40 mmHg) was maintained by returning 25-30% (intermediate-shock, IS) or 55-60% (late-shock, LS) of the shed blood. We resuscitated IS rats by reinfusion of all of the remaining shed blood and Ringer's lactate solution. Hepatic cellular Na and Cl increased and K decreased progressively with shock. Resuscitation of IS rats restored cell K and Cl but not Na to preshock levels. Em decreased from the control average value of -40 (mV) to -31 in IS and -19 in LS. Em was partially restored (-36 mV) after resuscitation. We evaluated changes in relative membrane permeability to Na and K (PNa/PK) with shock by assuming Em either to be a Na-K exchange diffusion potential or due to an unequally coupled movement of Na and K. These evaluations show a lack of effect of shock (IS, with or without resuscitation) on PNa/PK. Our observations are compatible with failure of an electrogenic Na pump in shock. This may be related to loss of hepatic cell volume regulation in shock.
mesh_terms: D000818:Animals; D001693:Biological Transport, Active; D001834:Body Water / Q000378:metabolism; D008099:Liver / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008564:Membrane Potentials; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D012771:Shock, Hemorrhagic / Q000378:metabolism / Q000503:physiopathology*; D012964:Sodium / Q000378:metabolism*
chemical_list: D012964:Sodium; D011188:Potassium