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Cerebral blood flow and oxidative metabolism during human endotoxemia

Publikation: Forskning - peer reviewTidsskriftartikel

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

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.
OriginalsprogEngelsk
TidsskriftJournal of Cerebral Blood Flow and Metabolism
Vol/bind22
Tidsskriftsnummer10
Sider (fra-til)1262-1270
Antal sider9
ISSN0271-678X
StatusUdgivet - 31 dec. 2002

ID: 162989576