Glucose clamping and cardiovascular function in endotoxic dogs.
Fasted mongrel dogs were anesthetized with pentobarbital sodium and instrumented for the continuous measurement of blood glucose (BG), a lead II electrocardiogram, and pressures in the left ventricle (LV), pulmonary artery, and aorta. Cardiac output was measured every 15 min using thermodilution and LV stroke work, and pulmonary and systemic resistances were calculated. After a 30-min pretreatment period, glucose clamping was initiated. The desired glucose levels were reached within 45 min (hypoglycemic 20 +/- 1 mg/dl, n = 11; normoglycemic 85 +/- 1, n = 7; hyperglycemic 156 +/- 3, n = 7). At this point dogs were treated with either endotoxin (8 mg/kg to 6 hypoglycemic, 4 normoglycemic, and 4 hyperglycemic) or saline (5 hypoglycemic, 3 normoglycemic, and 3 hyperglycemic). All infusions were terminated after 2 h glucose clamping, and all dogs were monitored either until death or for a maximum of 10 h. Hypoglycemic clamping curtailed survival in endotoxic dogs. Hyperglycemic clamping markedly prolonged survival. Normoglycemic clamping left survival time unchanged compared with untreated dogs. The effects of glucose clamping on cardiovascular function during endotoxic shock paralleled the effects on survival. Cardiovascular function was also depressed in hypoglycemic-clamped saline dogs. It is concluded that glucose dyshomeostasis may be a crucial factor in the development of fatal cardiovascular dysfunction and shock after endotoxin administration.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D002319:Cardiovascular System / Q000503:physiopathology*; D003250:Constriction / Q000379:methods; D004285:Dogs; D004731:Endotoxins / Q000494:pharmacology; D004926:Escherichia coli; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D012772:Shock, Septic / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology*
D001786:Blood Glucose; D004731:Endotoxins