Carbohydrate metabolism and the hemodynamic response to shock.
To investigate the temporal relationship of changes in carbohydrate metabolism to changes in the hemodynamic stability of the dog in protracted hemorrhagic shock, 30 animals were studied. Blood pressure was maintained at 60 mm Hg for 12 hr during which hemodynamic and metabolic parameters were studied. In early shock cardiac output was decreased and peripheral resistance increased. After 2 hr cardiac output began to increase and peripheral resistance began a progressive decline despite the continuing hypotensive state. Hemodynamic decompensation was essentially complete at 5 hr. There was early and marked mobilization of carbohydrate stores. Muscle glycogen was rapidly mobilized over a 5-hr period. Serum glucose and blood lactate levels rose and remained elevated for 8 hr. Amino acid degradation remained at high levels throughout the experimental period. Hemodynamic decompensation began well before significant depletion of carbohydrate stores and was complete well before the relative exhaustion of the available reserves.
D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose; D001794:Blood Pressure; D050260:Carbohydrate Metabolism; D002302:Cardiac Output; D004285:Dogs; D006003:Glycogen / Q000378:metabolism; D006439:Hemodynamics; D007773:Lactates / Q000097:blood; D008297:Male; D009132:Muscles / Q000378:metabolism; D010101:Oxygen Consumption; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D014655:Vascular Resistance
D000596:Amino Acids; D001786:Blood Glucose; D007773:Lactates; D006003:Glycogen