Effect of hemorrhagic shock on hepatic transmembrane potentials and intracellular electrolytes, in vivo

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Abstract
In vivo changes in hepatic cellular electrolytes and resting transmembrane potentials (Em) during hemorrhagic shock were investigated. 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% (intermediateshock, IS) or 55-60% (late-shock, LS) of the shed blood. IS rats were resuscitated 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 [resting membrane potential] 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. Changes in relative membrane permeability to Na and K (PNa/PK) with shock were evaluated 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 [ratio of permeability to Na and K]. The 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.