Effects of glucose infusion on cerebral cortical glucose and lactate concentrations during endotoxemia in rats

Sawa, T.; Okuda, C.; Harada, M.; Murakami, T.

Anesthesiology 77(4): 742-749

1992


ISSN/ISBN: 0003-3022
PMID: 1416172
Accession: 008568550

Download citation:  
Text
  |  
BibTeX
  |  
RIS

Article/Abstract emailed within 1 workday
Payments are secure & encrypted
Powered by Stripe
Powered by PayPal

Abstract
Hypoglycemia has been observed in several species before death from endotoxemia. Although several studies have emphasized the importance of maintaining brain glucose at normal concentration during endotoxemia, the effect of glucose infusion on cerebral glucose metabolism has not been studied. Accordingly, the effects of glucose infusion on interstitial glucose and lactate concentrations in the cerebral cortex during endotoxemia were studied in 22 Wistar rats. Cerebral glucose and lactate were measured a 30-min intervals for 4 h using microdialysis. Animals were divided into four groups: 1) saline-infused control (n = 5); 2) saline-infused endotoxemia (n = 7); 3) glucose-infused control (n = 5); and 4) glucose-infused endotoxemia (n = 5). In group 2 and 4, endotoxemia was induced by intravenous injection with Escherichia coli lipopolysaccharide B (5 mg cntdot 100 g-1). One hour after endotoxin administration, saline or 50% glucose was infused at a flow rate of 0.5 ml cntdot 100 g-1 cntdot h-1 for 3 h. Endotoxin induced a significant increase (P lt 0.005) in blood glucose in the saline-infused rats, which survived for 4 h (n = 5), from 91.6 +- 15.4 mg cntdot 100 ml-1 at baseline to 136.3 +- 23.3 mg cntdot 100 ml-1 (149%) at 1 h, followed by a gradual decrease (to 63% of the basal concentration at 4 h). Similar changes were observed in brain glucose (14.9 +- 1.9 mg cntdot 100 ml-1 baseline, 17% of baseline at 2 h, and 57% of baseline at 4 h). Although blood lactate significantly increased (P lt 0.05), from 0.82 +- 0.07 mEq cntdot l-1 at baseline to 3.07 +- 0.26 mEq cntdot l-1 (374%) at 4 h, brain lactate remained at the basal concentration (1.29 +- 0.14 mEq cntdot l-1) for 4 h. Glucose infusion from 1 h after endotoxin administration induced a significant increase (P lt 0.05) in both blood and brain glucose (485% and 377%, respectively, at 4 h). Blood lactate also markedly increased (590% at 4 h). Brain lactate also significantly increased after glucose infusion, but the increase was much less than that in the blood (160% at 2.5 h, peak value). We conclude that although glucose infusion effectively prevented the decrease in the brain glucose concentration during the hypoglycemic stage of endotoxemia, it caused mild lactate accumulation in the brain, in addition to systemic adverse effects, such as hyperglycemia and lactic acidosis.