Cerebral oxygen extraction and autoregulation during extracorporeal whole body hyperthermia in humans
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. Nineteen patients with chronic hepatitis C virus infection, not responding to interferon treatment, were...
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| Veröffentlicht in: | Anesthesiology (Philadelphia) 2004-05, Vol.100 (5), p.1101-1107 |
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| creator | CREMER, Olaf L DIEPHUIS, Jan C VAN SOEST, Hanneke VAESSEN, Paul H. B BRUENS, Marcel G. J HENNIS, Pim J KALKMAN, Cor J |
| description | 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.
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.
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.
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. |
| doi_str_mv | 10.1097/00000542-200405000-00011 |
| format | Article |
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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.
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.
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.</description><identifier>ISSN: 0003-3022</identifier><identifier>EISSN: 1528-1175</identifier><identifier>DOI: 10.1097/00000542-200405000-00011</identifier><identifier>PMID: 15114206</identifier><identifier>CODEN: ANESAV</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott</publisher><subject>Adult ; Anesthesia ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Biological and medical sciences ; Brain - blood supply ; Brain - drug effects ; Brain - physiology ; Confidence Intervals ; Energy Metabolism - drug effects ; Energy Metabolism - physiology ; Extracorporeal Circulation - methods ; Hepatitis C, Chronic - drug therapy ; Hepatitis C, Chronic - physiopathology ; Hepatitis C, Chronic - therapy ; Homeostasis - drug effects ; Homeostasis - physiology ; Humans ; Hyperthermia, Induced - methods ; Medical sciences ; Middle Aged ; Oxygen Consumption - drug effects ; Oxygen Consumption - physiology ; Pilot Projects ; Propofol - therapeutic use</subject><ispartof>Anesthesiology (Philadelphia), 2004-05, Vol.100 (5), p.1101-1107</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-9ed56ad134c8d166f3c55bee9c0ebf118435077091dbf0b80aae06b85dbc55423</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27926,27927</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15741538$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15114206$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CREMER, Olaf L</creatorcontrib><creatorcontrib>DIEPHUIS, Jan C</creatorcontrib><creatorcontrib>VAN SOEST, Hanneke</creatorcontrib><creatorcontrib>VAESSEN, Paul H. B</creatorcontrib><creatorcontrib>BRUENS, Marcel G. J</creatorcontrib><creatorcontrib>HENNIS, Pim J</creatorcontrib><creatorcontrib>KALKMAN, Cor J</creatorcontrib><title>Cerebral oxygen extraction and autoregulation during extracorporeal whole body hyperthermia in humans</title><title>Anesthesiology (Philadelphia)</title><addtitle>Anesthesiology</addtitle><description>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.
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.
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.
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.</description><subject>Adult</subject><subject>Anesthesia</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Biological and medical sciences</subject><subject>Brain - blood supply</subject><subject>Brain - drug effects</subject><subject>Brain - physiology</subject><subject>Confidence Intervals</subject><subject>Energy Metabolism - drug effects</subject><subject>Energy Metabolism - physiology</subject><subject>Extracorporeal Circulation - methods</subject><subject>Hepatitis C, Chronic - drug therapy</subject><subject>Hepatitis C, Chronic - physiopathology</subject><subject>Hepatitis C, Chronic - therapy</subject><subject>Homeostasis - drug effects</subject><subject>Homeostasis - physiology</subject><subject>Humans</subject><subject>Hyperthermia, Induced - methods</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Oxygen Consumption - drug effects</subject><subject>Oxygen Consumption - physiology</subject><subject>Pilot Projects</subject><subject>Propofol - therapeutic use</subject><issn>0003-3022</issn><issn>1528-1175</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkdtKxDAQhoMo7rr6CpIbvatmmqZNL2XxBII3el1ymO5W2mZNWnTf3uxaD4EQZvL9E_hCCAV2BawsrtluiSxNUsYyJmKRxA1wQOYgUpkAFOKQzGOPJ5yl6YychPAWy0JweUxmIACylOVzgkv0qL1qqfvcrrCn-Dl4ZYbG9VT1lqpxcB5XY6v2LTv6pl9NkPObeBejH2vXItXObul6u0E_rNF3jaJNT9djp_pwSo5q1QY8m84Feb27fVk-JE_P94_Lm6fE8BKGpEQrcmWBZ0ZayPOaGyE0YmkY6hpAZlywomAlWF0zLZlSyHIthdURzFK-IJffczfevY8YhqprgsG2VT26MVQFyLyQJURQfoPGuxA81tXGN53y2wpYtVNc_SiufhVXe8Uxej69MeoO7V9wchqBiwlQwai29qo3TfjHFRnEb-Bf16KF7A</recordid><startdate>20040501</startdate><enddate>20040501</enddate><creator>CREMER, Olaf L</creator><creator>DIEPHUIS, Jan C</creator><creator>VAN SOEST, Hanneke</creator><creator>VAESSEN, Paul H. B</creator><creator>BRUENS, Marcel G. J</creator><creator>HENNIS, Pim J</creator><creator>KALKMAN, Cor J</creator><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20040501</creationdate><title>Cerebral oxygen extraction and autoregulation during extracorporeal whole body hyperthermia in humans</title><author>CREMER, Olaf L ; DIEPHUIS, Jan C ; VAN SOEST, Hanneke ; VAESSEN, Paul H. B ; BRUENS, Marcel G. J ; HENNIS, Pim J ; KALKMAN, Cor J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-9ed56ad134c8d166f3c55bee9c0ebf118435077091dbf0b80aae06b85dbc55423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adult</topic><topic>Anesthesia</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Biological and medical sciences</topic><topic>Brain - blood supply</topic><topic>Brain - drug effects</topic><topic>Brain - physiology</topic><topic>Confidence Intervals</topic><topic>Energy Metabolism - drug effects</topic><topic>Energy Metabolism - physiology</topic><topic>Extracorporeal Circulation - methods</topic><topic>Hepatitis C, Chronic - drug therapy</topic><topic>Hepatitis C, Chronic - physiopathology</topic><topic>Hepatitis C, Chronic - therapy</topic><topic>Homeostasis - drug effects</topic><topic>Homeostasis - physiology</topic><topic>Humans</topic><topic>Hyperthermia, Induced - methods</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Oxygen Consumption - drug effects</topic><topic>Oxygen Consumption - physiology</topic><topic>Pilot Projects</topic><topic>Propofol - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CREMER, Olaf L</creatorcontrib><creatorcontrib>DIEPHUIS, Jan C</creatorcontrib><creatorcontrib>VAN SOEST, Hanneke</creatorcontrib><creatorcontrib>VAESSEN, Paul H. B</creatorcontrib><creatorcontrib>BRUENS, Marcel G. J</creatorcontrib><creatorcontrib>HENNIS, Pim J</creatorcontrib><creatorcontrib>KALKMAN, Cor J</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Anesthesiology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CREMER, Olaf L</au><au>DIEPHUIS, Jan C</au><au>VAN SOEST, Hanneke</au><au>VAESSEN, Paul H. B</au><au>BRUENS, Marcel G. J</au><au>HENNIS, Pim J</au><au>KALKMAN, Cor J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cerebral oxygen extraction and autoregulation during extracorporeal whole body hyperthermia in humans</atitle><jtitle>Anesthesiology (Philadelphia)</jtitle><addtitle>Anesthesiology</addtitle><date>2004-05-01</date><risdate>2004</risdate><volume>100</volume><issue>5</issue><spage>1101</spage><epage>1107</epage><pages>1101-1107</pages><issn>0003-3022</issn><eissn>1528-1175</eissn><coden>ANESAV</coden><abstract>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.
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.
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.
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.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott</pub><pmid>15114206</pmid><doi>10.1097/00000542-200405000-00011</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Anesthesia Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Biological and medical sciences Brain - blood supply Brain - drug effects Brain - physiology Confidence Intervals Energy Metabolism - drug effects Energy Metabolism - physiology Extracorporeal Circulation - methods Hepatitis C, Chronic - drug therapy Hepatitis C, Chronic - physiopathology Hepatitis C, Chronic - therapy Homeostasis - drug effects Homeostasis - physiology Humans Hyperthermia, Induced - methods Medical sciences Middle Aged Oxygen Consumption - drug effects Oxygen Consumption - physiology Pilot Projects Propofol - therapeutic use |
| title | Cerebral oxygen extraction and autoregulation during extracorporeal whole body hyperthermia in humans |
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