Mechanism of increased glucose uptake by skeletal muscle during E coli endotoxin shock in the dog.
Carbohydrate metabolism of skeletal muscle was studied during 2 mg/kg E coli endotoxin shock in dogs. During natural (free-flow) conditions, glucose uptake by the muscle increased markedly during 6 hours of shock. Increased glucose uptake occurred concomitant with muscle ischemia and hypoxia. However, when muscle blood flow was held constant, thereby preventing local muscle ischemia and hypoxia, glucose uptake by the gracilis muscle did not change during shock. These results implicate local muscle ischemia and/or hypoxia as the mediator(s) of the increased muscle glucose uptake during shock. Further studies demonstrated that local muscle hypoxia was the stimulus for increased glucose uptake by skeletal muscle during endotoxin shock, and muscle ischemia per se did not alter muscle glucose uptake. Since approximately 50% of body mass is composed of skeletal muscle, the contribution of this organ system in the hypoglycemia of endotoxin shock in the dog may be substantial.
D000818:Animals; D001427:Bacterial Toxins / Q000633:toxicity; D004285:Dogs; D004926:Escherichia coli; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006439:Hemodynamics; D000860:Hypoxia / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism; D008297:Male; D009132:Muscles / Q000378:metabolism*; D012772:Shock, Septic / Q000378:metabolism*
D001427:Bacterial Toxins; D005947:Glucose