Blood lactate and catecholamine levels in the carbon monoxide-exposed rat: the response to elevated glucose.
Previous studies have shown that elevated blood glucose is detrimental to the outcome in acute carbon monoxide (CO) poisoning. The present goals were to characterize the blood lactate and catecholamine changes and to determine whether elevated blood glucose results in increases in the levels of these substances. Two groups of adult Sprague-Dawley, Levine-prepared, female rats (n = 22 each) were exposed to 2400 ppm CO for 90 min: one group received nothing (CO alone), while the other group was infused with a 50% glucose solution (4 ml/kg) (CO + glucose). The usual hypothermia, hypotension, bradycardia and hemoconcentration associated with acute severe CO poisoning were observed. Survival rates were 68% and 54% in the CO alone and CO + glucose groups, respectively. Arterial blood pressure tended to decline more in rats that died; the difference was significant in the CO + glucose group. In the CO alone group, plasma glucose concentration was significantly lower after CO exposure in rats that died than in survivors (35 +/- 15 vs. 99 +/- 16 mg/dl). In the CO + glucose group, glucose concentration was significantly higher after 45 min in rats that died (d) than in survivors (s) (447 +/- 29 vs. 324 +/- 31 mg/dl). Elevated blood glucose in the CO + glucose group failed to significantly increase blood lactate; however, lactate tended to be higher in rats that died in both groups [CO alone group: 175 +/- 17 (d) vs. 138 +/- 9 (s); CO + glucose group: 154 +/- 10 (d) vs. 143 +/- 8 (s)]. Plasma epinephrine and norepinephrine increased significantly 6-10-fold and 2-6-fold in each of the two groups, respectively; however, catecholamine levels were not related to either the administration of glucose or survival. With regard to CO poisoning in this animal model, the results do not support the hypotheses that elevated blood glucose exacerbates the increase in blood lactate, that increased catecholamine increases glucose, or that greater CO-induced hypoglycemia results from increased lactate production. The results do show that death is related to abnormally high or low blood glucose, but that it is not due to higher blood lactate or catecholamine levels.
Sutariya
B B
BB
Department of Biological Sciences, Wayne State University School of Medicine, Detroit, MI 48201.
Penney
D G
DG
Dunbar
J C
JC
Swanson
C J
CJ
D000818:Animals; D001786:Blood Glucose / Q000032:analysis*; D001794:Blood Pressure; D001831:Body Temperature; D002249:Carbon Monoxide Poisoning / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D002395:Catecholamines / Q000097:blood*; D004195:Disease Models, Animal; D004837:Epinephrine / Q000097:blood; D005260:Female; D005947:Glucose / Q000627:therapeutic use; D006339:Heart Rate; D006400:Hematocrit; D006943:Hyperglycemia / Q000097:blood*; D007003:Hypoglycemia / Q000209:etiology; D007773:Lactates / Q000097:blood*; D009638:Norepinephrine / Q000097:blood; D011897:Random Allocation; D051381:Rats; D011919:Rats, Inbred Strains
D001786:Blood Glucose; D002395:Catecholamines; D007773:Lactates; D005947:Glucose; D009638:Norepinephrine; D004837:Epinephrine