Ion transport in circulatory and/or septic shock

Abstract

This review surveys investigations of membrane ion transport in animals in hemorrhagic, endotoxic, or bacteremic shock. The focus of the review is on ion transport studies in the skeletal muscle and liver. Skeletal muscle Na+-K+ transport alterations have been shown during the induction of shock via hemorrhage, endotoxin, or live Gram-negative bacteria in the rodent, canine, and primate species. These alterations include impairment of active cellular K+ accumulation, increased permeability to Na+ and Cl-, and membrane depolarization. The ion transport alterations in the skeletal muscle are compatible with movement of extracellular fluid into the intracellular compartment. Such fluid movements can potentially lead to decreases in circulating plasma volume and thus to circulatory deficits in shock. Studies in the liver of rats subjected to hemorrhagic or endotoxic shock indicated the failure of electrogenic Na+ pump. Although the hepatic cellular membrane permeability to Na+ relative to permeability to K+ appeared unaltered in hemorrhagic shock, endotoxic shock caused an increase in permeability to Na+. Hepatic cellular Ca+ regulation also appeared to be adversely affected during endotoxic shock. Alterations in hepatic Na+-K+ transport and Ca+ regulation could contribute to impairment in hepatic glucose production during shock. Although mechanisms of altered membrane ion transport during shock states remain unknown, such changes could occur prior to any substantial loss of cellular metabolic energy.