Effects of glucose-insulin-potassium (GIK) on the position of the oxyhemoglobin dissociation curve, 2.3-diphosphoglycerate, and oxygen consumption in canine endotoxin shock.

The effects of glucose-insulin-potassium (GIK) on hemodynamics, oxygen transport, P50, 2,3-diphosphoglycerate (2.3-DPG), and adenosine triphosphate (ATP) were evaluated in canine endotoxin shock. Ten dogs were studied under general anesthesia and controlled ventilation. Shock was induced with Escherichia coli endotoxin (1.5 mg/kg body wt). Thereafter two groups of five dogs each were formed by randomization. The one group received GIK (glucose 50%, 2 g/kg, insulin 3 U/kg, and 10 mmole K) in the period between 90 and 120 min after endotoxin. The other group received an equal amount of NaCl infusion and served as a control group. Observations were completed at 180 min after endotoxin. GIK resulted in a significant increase of cardiac output, stroke volume, mean arterial pressure, and oxygen consumption. Serum phosphate levels decreased. No changes were observed of P50 in vitro (at 37 degrees C and pH 7.40) and of P50 in vivo, nor of 2.3-DPG and ATP in the red cells. The data suggest that the increased oxygen consumption after GIK in canine endotoxin shock is caused only by improvement of cardiac output and oxygen availability and not by an effect on oxygen unloading capacity of hemoglobin.