Glucose dyshomeostasis and cardiovascular failure in endotoxic dogs.
Fasted mongrel dogs were anesthetized with pentobarbital sodium and instrumented for the on-line measurement of blood glucose (BG), a lead II electrocardiogram, and pressures in the left ventricle and pulmonary and systemic artery concomitant with on-line monitoring of BG. Serum insulin was measured by radioimmunoassay, and cardiac output (CO) was determined by thermodilution. Stroke work (SW) and pulmonary and systemic resistances were calculated. After a 30-min control period dogs were treated with Escherichia coli endotoxin (E) or normal saline (S) and then observed for 10 h or until death. Preinjection control BG was maintained in S dogs, and early hyperglycemia (H) was observed in six dogs; in contrast 10 E dogs showed no hyperglycemia (NH). During the late stages all E dogs were markedly hypoglycemic. In both groups of E dogs an early hyperinsulinemia occurred. CO and SW were depressed in both groups of E dogs. These variables were significantly lower in NH than in H dogs. Pulmonary and systemic resistance progressively increased in NH dogs after endotoxin administration. The results suggest that the ability to increase blood glucose levels after endotoxin injection is important for the maintenance of cardiovascular function. Glucose dyshomeostasis leading to hypoglycemia, however, may be a factor in the development of endotoxic cardiovascular failure.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D004731:Endotoxins / Q000494:pharmacology; D004926:Escherichia coli; D005260:Female; D006706:Homeostasis; D008297:Male; D012772:Shock, Septic / Q000209:etiology*; D014655:Vascular Resistance / Q000187:drug effects
D001786:Blood Glucose; D004731:Endotoxins