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. CONCLUSION: 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.
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. CONCLUSION: 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.
Authors: Monica S Vavilala; M Sean Kincaid; Saipin L Muangman; Pilar Suz; Irene Rozet; Arthur M Lam Journal: Pediatr Res Date: 2005-09 Impact factor: 3.756
Authors: Pavel S Yarmolenko; Eui Jung Moon; Chelsea Landon; Ashley Manzoor; Daryl W Hochman; Benjamin L Viglianti; Mark W Dewhirst Journal: Int J Hyperthermia Date: 2011 Impact factor: 3.914
Authors: Krishma Adatia; Romergryko G Geocadin; Ryan Healy; Wendy Ziai; Luciano Ponce-Mejia; Mirinda Anderson-White; Dhaval Shah; Batya R Radzik; Caitlin Palmisano; Charles W Hogue; Charles Brown; Lucia Rivera-Lara Journal: Crit Care Med Date: 2018-08 Impact factor: 7.598
Authors: Monica S Vavilala; Nuj Tontisirin; Yuthana Udomphorn; William Armstead; Jerry J Zimmerman; Randall Chesnut; Arthur M Lam Journal: Neurocrit Care Date: 2008 Impact factor: 3.210
Authors: Patrick Schramm; Klaus Ulrich Klein; Lena Falkenberg; Manfred Berres; Dorothea Closhen; Konrad J Werhahn; Matthias David; Christian Werner; Kristin Engelhard Journal: Crit Care Date: 2012-10-04 Impact factor: 9.097
Authors: Gerben Lassche; Tim Frenzel; Marcel H Mignot; Marianne A Jonker; Johannes G van der Hoeven; Carla M L van Herpen; Gert Jan Scheffer Journal: Physiol Rep Date: 2020-02