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Am J Physiol Endocrinol Metab 254: E16-E22, 1988;
0193-1849/88 $5.00
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AJP - Endocrinology and Metabolism, Vol 254, Issue 1 E16-E22, Copyright © 1988 by American Physiological Society

ARTICLES

Adrenergic blockade does not abolish elevated glucose turnover during bacterial infection

D. M. Hargrove, G. J. Bagby, C. H. Lang and J. J. Spitzer
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.

Infusions of adrenergic antagonists were used to investigate the role of catecholamines in infection-induced elevations of glucose kinetics. Infection was produced in conscious catheterized rats by repeated subcutaneous injections of live Escherichia coli over 24 h. Glucose kinetics were measured by the constant intravenous infusion of [6-3H]- and [U-14C]glucose. Compared with noninfected rats, infected animals were hyperthermic (+1.4 degrees C) and showed increased rates of glucose appearance (45%), clearance (43%), and recycling (140%) as well as mild hyperlacticacidemia. Plasma catecholamine concentrations were increased by 50-70% in the infected rats, but there were no differences in plasma glucagon, corticosterone, and insulin levels. Adrenergic blockade was produced by primed constant infusion of both propranolol (beta-blocker) and phentolamine (alpha-blocker). A 2-h administration of adrenergic antagonists did not attenuate the elevated glucose kinetics or plasma lactate concentration in the infected rats, although it abolished the hyperthermia. In a second experiment, animals were infused with propranolol and phentolamine beginning 1 h before the first injection of E. coli and throughout the course of infection. Continuous adrenergic blockade failed to attenuate infection-induced elevations in glucose kinetics and plasma lactate. These results indicate that the adrenergic system does not mediate the elevated glucose metabolism observed in this mild model of infection.


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