Cerebral blood flow and oxidative metabolism during human endotoxemia

Kirsten Møller; Gitte Irene Strauss; Jesper Qvist; Lise Fonsmark; Karen Birgitte Moos Knudsen; Fin Stolze Larsen; Karen Suarez Krabbe; Peter Skinhøj; Bente Klarlund Pedersen

Cerebral blood flow and oxidative metabolism during human endotoxemia

Kirsten Møller, Gitte Irene Strauss, Jesper Qvist, Lise Fonsmark, Karen Birgitte Moos Knudsen, Fin Stolze Larsen, Karen Suarez Krabbe, Peter Skinhøj, Bente Klarlund Pedersen

62 Citationer (Scopus)

Abstract

The proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), has been suggested to mediate septic encephalopathy through an effect on cerebral blood flow (CBF) and metabolism. The effect of an intravenous bolus of endotoxin on global CBF, metabolism, and net flux of cytokines and catecholamines was investigated in eight healthy young volunteers. Cerebral blood flow was measured by the Kety-Schmidt technique at baseline (during normocapnia and voluntary hyperventilation for calculation of subject-specific cerebrovascular CO reactivity), and 90 minutes after an intravenous bolus of a reference endotoxin. Arterial TNF-alpha peaked at 90 minutes, coinciding with a peak in subjective symptoms. At this time, CBF and Paco were significantly reduced compared to baseline; the CBF decrease was readily explained by hypocapnia. The cerebral metabolic rate of oxygen remained unchanged, and the net cerebral flux of TNF-alpha, interleukin (IL)-1beta, and IL-6 did not differ significantly from zero. Thus, high circulating levels of TNF-alpha during human endotoxemia do not induce a direct reduction in cerebral oxidative metabolism.

Originalsprog	Engelsk
Tidsskrift	Journal of Cerebral Blood Flow and Metabolism
Vol/bind	22
Udgave nummer	10
Sider (fra-til)	1262-1270
Antal sider	9
ISSN	0271-678X
Status	Udgivet - 31 dec. 2002

Citationsformater

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title = "Cerebral blood flow and oxidative metabolism during human endotoxemia",

abstract = "The proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), has been suggested to mediate septic encephalopathy through an effect on cerebral blood flow (CBF) and metabolism. The effect of an intravenous bolus of endotoxin on global CBF, metabolism, and net flux of cytokines and catecholamines was investigated in eight healthy young volunteers. Cerebral blood flow was measured by the Kety-Schmidt technique at baseline (during normocapnia and voluntary hyperventilation for calculation of subject-specific cerebrovascular CO reactivity), and 90 minutes after an intravenous bolus of a reference endotoxin. Arterial TNF-alpha peaked at 90 minutes, coinciding with a peak in subjective symptoms. At this time, CBF and Paco were significantly reduced compared to baseline; the CBF decrease was readily explained by hypocapnia. The cerebral metabolic rate of oxygen remained unchanged, and the net cerebral flux of TNF-alpha, interleukin (IL)-1beta, and IL-6 did not differ significantly from zero. Thus, high circulating levels of TNF-alpha during human endotoxemia do not induce a direct reduction in cerebral oxidative metabolism.",

author = "Kirsten M{\o}ller and Strauss, {Gitte Irene} and Jesper Qvist and Lise Fonsmark and Knudsen, {Karen Birgitte Moos} and Larsen, {Fin Stolze} and {Suarez Krabbe}, Karen and Peter Skinh{\o}j and Pedersen, {Bente Klarlund}",

year = "2002",

month = dec,

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language = "English",

volume = "22",

pages = "1262--1270",

journal = "Journal of Cerebral Blood Flow and Metabolism",

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TY - JOUR

T1 - Cerebral blood flow and oxidative metabolism during human endotoxemia

AU - Møller, Kirsten

AU - Strauss, Gitte Irene

AU - Qvist, Jesper

AU - Fonsmark, Lise

AU - Knudsen, Karen Birgitte Moos

AU - Larsen, Fin Stolze

AU - Suarez Krabbe, Karen

AU - Skinhøj, Peter

AU - Pedersen, Bente Klarlund

PY - 2002/12/31

Y1 - 2002/12/31

N2 - The proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), has been suggested to mediate septic encephalopathy through an effect on cerebral blood flow (CBF) and metabolism. The effect of an intravenous bolus of endotoxin on global CBF, metabolism, and net flux of cytokines and catecholamines was investigated in eight healthy young volunteers. Cerebral blood flow was measured by the Kety-Schmidt technique at baseline (during normocapnia and voluntary hyperventilation for calculation of subject-specific cerebrovascular CO reactivity), and 90 minutes after an intravenous bolus of a reference endotoxin. Arterial TNF-alpha peaked at 90 minutes, coinciding with a peak in subjective symptoms. At this time, CBF and Paco were significantly reduced compared to baseline; the CBF decrease was readily explained by hypocapnia. The cerebral metabolic rate of oxygen remained unchanged, and the net cerebral flux of TNF-alpha, interleukin (IL)-1beta, and IL-6 did not differ significantly from zero. Thus, high circulating levels of TNF-alpha during human endotoxemia do not induce a direct reduction in cerebral oxidative metabolism.

AB - The proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), has been suggested to mediate septic encephalopathy through an effect on cerebral blood flow (CBF) and metabolism. The effect of an intravenous bolus of endotoxin on global CBF, metabolism, and net flux of cytokines and catecholamines was investigated in eight healthy young volunteers. Cerebral blood flow was measured by the Kety-Schmidt technique at baseline (during normocapnia and voluntary hyperventilation for calculation of subject-specific cerebrovascular CO reactivity), and 90 minutes after an intravenous bolus of a reference endotoxin. Arterial TNF-alpha peaked at 90 minutes, coinciding with a peak in subjective symptoms. At this time, CBF and Paco were significantly reduced compared to baseline; the CBF decrease was readily explained by hypocapnia. The cerebral metabolic rate of oxygen remained unchanged, and the net cerebral flux of TNF-alpha, interleukin (IL)-1beta, and IL-6 did not differ significantly from zero. Thus, high circulating levels of TNF-alpha during human endotoxemia do not induce a direct reduction in cerebral oxidative metabolism.

M3 - Journal article

SN - 0271-678X

VL - 22

SP - 1262

EP - 1270

JO - Journal of Cerebral Blood Flow and Metabolism

JF - Journal of Cerebral Blood Flow and Metabolism

IS - 10

ER -