Adrenergic blockade does not abolish elevated glucose turnover during bacterial infection

D. M. Hargrove, G. J. Bagby, C. H. Lang, J. J. Spitzer

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

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°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 (β-blocker) and phentolamine (α-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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume254
Issue number1
StatePublished - Jan 1 1988

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Bacterial Infections
Adrenergic Agents
Glucose
Infection
Adrenergic Antagonists
Phentolamine
Propranolol
Catecholamines
Lactic Acid
Escherichia coli
Recycling
Subcutaneous Injections
Corticosterone
Glucagon
Intravenous Infusions
Fever
Insulin
Injections

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)

Cite this

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title = "Adrenergic blockade does not abolish elevated glucose turnover during bacterial infection",
abstract = "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°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 (β-blocker) and phentolamine (α-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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Adrenergic blockade does not abolish elevated glucose turnover during bacterial infection. / Hargrove, D. M.; Bagby, G. J.; Lang, C. H.; Spitzer, J. J.

In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 254, No. 1, 01.01.1988.

Research output: Contribution to journalArticle

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