Cerebral oxygen extraction and autoregulation during extracorporeal whole body hyperthermia in humans.
BACKGROUND
The effects of hyperthermia on the human brain are incompletely understood. This study assessed the effects of whole body hyperthermia on cerebral oxygen extraction and autoregulation in humans.


METHODS
Nineteen patients with chronic hepatitis C virus infection, not responding to interferon treatment, were subjected to experimental therapy with extracorporeal whole body hyperthermia at 41.8 degrees C for 120 min under propofol anesthesia (23 sessions total). During treatment series A (13 sessions), end-tidal carbon dioxide was allowed to increase during heating. During series B (10 sessions), end-tidal carbon dioxide was maintained approximately constant. Cerebral oxygen extraction (arterial to jugular venous difference of oxygen content) and middle cerebral artery blood flow velocity were continuously measured. Cerebral pressure-flow autoregulation was assessed by static tests using phenylephrine infusion and by assessing the transient hyperemic response to carotid compression and release.


RESULTS
For treatment series A, cerebral oxygen extraction decreased 2.2-fold and cerebral blood flow velocity increased 2.0-fold during heating. For series B, oxygen extraction decreased 1.6-fold and flow velocity increased 1.5-fold. Jugular venous oxygen saturation and lactate measurements did not indicate cerebral ischemia at any temperature. Static autoregulation test results indicated loss of cerebrovascular reactivity during hyperthermia for both series A and series B. The transient hyperemic response ratio did not decrease until the temperature reached approximately 40 degrees C. Per degree Celsius temperature increase, the transient hyperemic response ratio decreased 0.07 (95% confidence interval, 0.05-0.09; P = 0.000). This association remained after adjustment for variations in arterial partial pressure of carbon dioxide, mean arterial pressure, and propofol blood concentration.


CONCLUSIONS
Profound hyperthermia during propofol anesthesia is associated with decreased cerebral oxygen extraction, increased cerebral blood flow velocity, and impaired pressure-flow autoregulation, indicating transient partial vasoparalysis.
Cremer
Olaf L
OL
University Medical Center Utrecht E03.511, P. O. Box 85500, 3508 GA Utrecht, The Netherlands. o.l.cremer@azu.nl
Diephuis
Jan C
JC
van Soest
Hanneke
H
Vaessen
Paul H B
PH
Bruens
Marcel G J
MG
Hennis
Pim J
PJ
Kalkman
Cor J
CJ
D000328:Adult; D001921:Brain / Q000098:blood supply / Q000187:drug effects / Q000502:physiology*; D016001:Confidence Intervals; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology; D005112:Extracorporeal Circulation / Q000379:methods*; D019698:Hepatitis C, Chronic / Q000188:drug therapy / Q000503:physiopathology / Q000628:therapy; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D006979:Hyperthermia, Induced / Q000379:methods*; D008875:Middle Aged; D010101:Oxygen Consumption / Q000187:drug effects / Q000502:physiology*; D010865:Pilot Projects; D015742:Propofol / Q000627:therapeutic use
D015742:Propofol