Metabolic effect of the neuroendocrine stress response

U. Suchner, Michael Rothkopf

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The neuroendocrine response to stress is initiated by afferent stimuli, such as pain, hemodynamic alterations, core temperature changes, circulating substrate levels, and emotional reaction. This information is processed by the central nervous system, and an efferent response is initiated through the hypothalamus. Rapid effects are mediated through the hypothalamic-autonomic-adrenal axis, whereas effects mediated through the hypothalamic-pituitary axis are slower and of longer duration. Stimulation along these pathways produces profound changes in metabolism. Hepatic glucose output is increased, whereas peripheral use of glucose is suppressed by the actions of cortisol, catecholamines, growth hormone, and glucagon. This metabolic adjustment would appear to have been orchestrated to achieve the mobilization of peripheral fuel stores so that glucose-dependent tissues such as the central nervous system, blood cells, and wound tissue are not deprived. More remains to be learned about this important area and its effects on the outcome of critical illness.

Original languageEnglish (US)
Pages (from-to)1-22
Number of pages22
JournalAnesthesiology Clinics of North America
Volume6
Issue number1
StatePublished - Jan 1 1988
Externally publishedYes

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Glucose
Central Nervous System
Glucagon
Critical Illness
Growth Hormone
Hypothalamus
Catecholamines
Hydrocortisone
Blood Cells
Hemodynamics
Pain
Temperature
Liver
Wounds and Injuries

All Science Journal Classification (ASJC) codes

  • Anesthesiology and Pain Medicine

Cite this

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Metabolic effect of the neuroendocrine stress response. / Suchner, U.; Rothkopf, Michael.

In: Anesthesiology Clinics of North America, Vol. 6, No. 1, 01.01.1988, p. 1-22.

Research output: Contribution to journalArticle

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