Effect of hemorrhagic shock on hepatic transmembrane potentials and intracellular electrolytes, in vivo.
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.
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*
D012964:Sodium; D011188:Potassium