(passage)

The myocellular transmembrance Na+ gradient is important for proper cellular function. During septic shock, disruption of Na+ homeostasis often occurs and leads to decreased membrane potential and increased intracellular Na+. It has been found that failure of cellular energy metabolism is a common symptom in septic patients who do not respond to therapeutics. Because normal intracellular levels of Na+ are maintained by the Na+K+ ATPase, it is important to inderstand how metabolic energy production is linked to cation transport.

Researchers are interested inwhether the energy used for iontransport is derived from glycolysis or oxidative phosphorylation. This information would provide a vetter understanding of myocellular damage that occurs during critical illness. Experiments wereconducted to evaluate the effects of qlyclytic inhibition on cellular Na+ and K+ concentrations and lactate production in rat skeletal myocytes.

Rat skeletal muscle fibers were extracted and incubated in normal media (Control), glucose-free media (G(-)),and qlucose-free media wuth various concentrations of the glycolytic inhibitor iodoacetate (IAA). IAA directly prevents thr formation of 1,3-bisphosphoglycerate. After one hour in the media, the muscle tissues were assayed for intracellular Na+ snd K+ content and lactate production. cellular viability was determined by measuring the amount of lactate dehydroqenase (LDH) released, as LDH release is an indicater of cell death.

The results ate displayed in Figure 1.

Figure1 “Effects of glycolytic inhibition on intracellular Na+ and k+ content and lactate production with cellular viability measured by LDH refease. (Note: The *indicates p < 0.05 versus control.)