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Reductions in cerebral blood flow during passive heat stress in humans: partitioning the mechanisms
Non‐technical summary Heat stress reduces brain blood flow and impairs orthostatic tolerance. Brain blood flow is largely controlled by the partial pressure of arterial . Indeed, hyperthermia‐induced over‐breathing and related reductions in arterial account for ∼50% of the reduction in brain blood...
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Published in: | The Journal of physiology 2011-08, Vol.589 (16), p.4053-4064 |
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description | Non‐technical summary Heat stress reduces brain blood flow and impairs orthostatic tolerance. Brain blood flow is largely controlled by the partial pressure of arterial . Indeed, hyperthermia‐induced over‐breathing and related reductions in arterial account for ∼50% of the reduction in brain blood flow. This investigation tested the unique hypothesis that the distribution of cardiac output during heat stress (challenged by thermoregulatory increases in skin blood flow and sweat loss) contributes to the remaining 50%. We show that cardiac output is not related to brain blood flow, but rather arterial plays a much larger role than previously suggested. These findings help us understand the mechanisms relating heat stress with an increased likelihood of fainting, and are also relevant to pathological conditions that are accompanied by elevations in body temperature.
Cerebral blood flow (CBF) is reduced during passive heat stress, with 50% of this reduction associated with hyperventilatory‐induced hypocapnia and subsequent cerebral vasoconstriction. It remains unknown, however, what other factors may contribute to the remaining 50%. We tested the hypothesis that the distribution of cardiac output plays an important role in maintaining cerebral perfusion during mild and severe heat stress. Middle cerebral artery and posterior cerebral artery blood flow velocity (MCAv and PCAv; transcranial Doppler) and left ventricular end‐diastolic and end‐systolic volumes (2‐D echocardiography) were measured under conditions of normothermia and mild and severe passive heat stress (core temperature +0.8 ± 0.1°C (Protocol I; n= 10) and 1.8 ± 0.1°C (Protocol II; n= 8) above baseline). Venous return was manipulated by passive tilt table positioning (30 deg head‐down tilt (HDT) and 30 deg head‐up tilt (HUT)). Measurements were made under poikilocapnic and isocapnic conditions. Protocol I consisted of mild heat stress which resulted in small reductions in end‐tidal CO2 (−5.6 ± 3.5%), MCAv/PCAv (−7.3 ± 2.3% and −10.3 ± 2.9%, respectively) and stroke volume (−8.5 ± 4.2%); while end‐diastolic volume was significantly reduced (−16.9 ± 4.0%) and cardiac output augmented (17.2 ± 7.4%). During mild heat stress, CBF was related to left ventricular end‐diastolic volume (MCAv, r2= 0.81; PCAv, r2= 0.83; P < 0.05) and stroke volume (MCAv, r2= 0.38; PCAv, r2= 0.43), but not with cardiac output. Protocol II consisted of severe heat stress which resulted in much greater reductions in end‐tidal |
doi_str_mv | 10.1113/jphysiol.2011.212118 |
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Cerebral blood flow (CBF) is reduced during passive heat stress, with 50% of this reduction associated with hyperventilatory‐induced hypocapnia and subsequent cerebral vasoconstriction. It remains unknown, however, what other factors may contribute to the remaining 50%. We tested the hypothesis that the distribution of cardiac output plays an important role in maintaining cerebral perfusion during mild and severe heat stress. Middle cerebral artery and posterior cerebral artery blood flow velocity (MCAv and PCAv; transcranial Doppler) and left ventricular end‐diastolic and end‐systolic volumes (2‐D echocardiography) were measured under conditions of normothermia and mild and severe passive heat stress (core temperature +0.8 ± 0.1°C (Protocol I; n= 10) and 1.8 ± 0.1°C (Protocol II; n= 8) above baseline). Venous return was manipulated by passive tilt table positioning (30 deg head‐down tilt (HDT) and 30 deg head‐up tilt (HUT)). Measurements were made under poikilocapnic and isocapnic conditions. Protocol I consisted of mild heat stress which resulted in small reductions in end‐tidal CO2 (−5.6 ± 3.5%), MCAv/PCAv (−7.3 ± 2.3% and −10.3 ± 2.9%, respectively) and stroke volume (−8.5 ± 4.2%); while end‐diastolic volume was significantly reduced (−16.9 ± 4.0%) and cardiac output augmented (17.2 ± 7.4%). During mild heat stress, CBF was related to left ventricular end‐diastolic volume (MCAv, r2= 0.81; PCAv, r2= 0.83; P < 0.05) and stroke volume (MCAv, r2= 0.38; PCAv, r2= 0.43), but not with cardiac output. Protocol II consisted of severe heat stress which resulted in much greater reductions in end‐tidal CO2 (−87.5 ± 31.5%) and CBF (MCAv, −36.4 ± 6.1%; PCAv, −30.1 ± 4.8%; P < 0.01 for all variables), while end‐diastolic volume and stroke volume decreased to a similar extent as for mild heat stress. Importantly, isocapnia restored MCAv and PCAv back to normothermic baseline. This investigation therefore produced two novel findings: first, that venous return and stroke volume are related to CBF during mild heat stress; and second, that hyperventilatory hypocapnia has a major influence on CBF during severe passive heat stress.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.2011.212118</identifier><identifier>PMID: 21690194</identifier><identifier>CODEN: JPHYA7</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Blood Flow Velocity - physiology ; Blood Pressure - physiology ; Body Temperature - physiology ; Cerebrovascular Circulation - physiology ; Heart Rate - physiology ; Heat Stress Disorders - physiopathology ; Heat Stress Disorders - prevention & control ; Heat-Shock Response - physiology ; Humans ; Indexing in process ; Integrative ; Male ; Severity of Illness Index ; Stroke Volume - physiology ; Young Adult</subject><ispartof>The Journal of physiology, 2011-08, Vol.589 (16), p.4053-4064</ispartof><rights>2011 The Authors. Journal compilation © 2011 The Physiological Society</rights><rights>Journal compilation © 2011 The Physiological Society 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5848-e69d9da3d3eba20e2d26dc0d083fe6dbd96fc1de33ad83b8081b11616ff2f09e3</citedby><cites>FETCH-LOGICAL-c5848-e69d9da3d3eba20e2d26dc0d083fe6dbd96fc1de33ad83b8081b11616ff2f09e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3180002/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3180002/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21690194$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nelson, Michael D.</creatorcontrib><creatorcontrib>Haykowsky, Mark J.</creatorcontrib><creatorcontrib>Stickland, Michael K.</creatorcontrib><creatorcontrib>Altamirano‐Diaz, Luis A.</creatorcontrib><creatorcontrib>Willie, Christopher K.</creatorcontrib><creatorcontrib>Smith, Kurt J.</creatorcontrib><creatorcontrib>Petersen, Stewart R.</creatorcontrib><creatorcontrib>Ainslie, Philip N.</creatorcontrib><title>Reductions in cerebral blood flow during passive heat stress in humans: partitioning the mechanisms</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>Non‐technical summary Heat stress reduces brain blood flow and impairs orthostatic tolerance. Brain blood flow is largely controlled by the partial pressure of arterial . Indeed, hyperthermia‐induced over‐breathing and related reductions in arterial account for ∼50% of the reduction in brain blood flow. This investigation tested the unique hypothesis that the distribution of cardiac output during heat stress (challenged by thermoregulatory increases in skin blood flow and sweat loss) contributes to the remaining 50%. We show that cardiac output is not related to brain blood flow, but rather arterial plays a much larger role than previously suggested. These findings help us understand the mechanisms relating heat stress with an increased likelihood of fainting, and are also relevant to pathological conditions that are accompanied by elevations in body temperature.
Cerebral blood flow (CBF) is reduced during passive heat stress, with 50% of this reduction associated with hyperventilatory‐induced hypocapnia and subsequent cerebral vasoconstriction. It remains unknown, however, what other factors may contribute to the remaining 50%. We tested the hypothesis that the distribution of cardiac output plays an important role in maintaining cerebral perfusion during mild and severe heat stress. Middle cerebral artery and posterior cerebral artery blood flow velocity (MCAv and PCAv; transcranial Doppler) and left ventricular end‐diastolic and end‐systolic volumes (2‐D echocardiography) were measured under conditions of normothermia and mild and severe passive heat stress (core temperature +0.8 ± 0.1°C (Protocol I; n= 10) and 1.8 ± 0.1°C (Protocol II; n= 8) above baseline). Venous return was manipulated by passive tilt table positioning (30 deg head‐down tilt (HDT) and 30 deg head‐up tilt (HUT)). Measurements were made under poikilocapnic and isocapnic conditions. Protocol I consisted of mild heat stress which resulted in small reductions in end‐tidal CO2 (−5.6 ± 3.5%), MCAv/PCAv (−7.3 ± 2.3% and −10.3 ± 2.9%, respectively) and stroke volume (−8.5 ± 4.2%); while end‐diastolic volume was significantly reduced (−16.9 ± 4.0%) and cardiac output augmented (17.2 ± 7.4%). During mild heat stress, CBF was related to left ventricular end‐diastolic volume (MCAv, r2= 0.81; PCAv, r2= 0.83; P < 0.05) and stroke volume (MCAv, r2= 0.38; PCAv, r2= 0.43), but not with cardiac output. Protocol II consisted of severe heat stress which resulted in much greater reductions in end‐tidal CO2 (−87.5 ± 31.5%) and CBF (MCAv, −36.4 ± 6.1%; PCAv, −30.1 ± 4.8%; P < 0.01 for all variables), while end‐diastolic volume and stroke volume decreased to a similar extent as for mild heat stress. Importantly, isocapnia restored MCAv and PCAv back to normothermic baseline. This investigation therefore produced two novel findings: first, that venous return and stroke volume are related to CBF during mild heat stress; and second, that hyperventilatory hypocapnia has a major influence on CBF during severe passive heat stress.</description><subject>Adult</subject><subject>Blood Flow Velocity - physiology</subject><subject>Blood Pressure - physiology</subject><subject>Body Temperature - physiology</subject><subject>Cerebrovascular Circulation - physiology</subject><subject>Heart Rate - physiology</subject><subject>Heat Stress Disorders - physiopathology</subject><subject>Heat Stress Disorders - prevention & control</subject><subject>Heat-Shock Response - physiology</subject><subject>Humans</subject><subject>Indexing in process</subject><subject>Integrative</subject><subject>Male</subject><subject>Severity of Illness Index</subject><subject>Stroke Volume - physiology</subject><subject>Young Adult</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNqNkU9v1DAQxS0EokvhGyAUiQNcsszYTtbmgIQq_qoSCJWz5cSTxqskXuyk1X57vGxbAQfEaQ7ze08z7zH2FGGNiOLVdtfvkw_DmgPimiNHVPfYCmWty81Gi_tsBcB5KTYVnrBHKW0BUIDWD9kJx1oDarli7TdySzv7MKXCT0VLkZpoh6IZQnBFN4Trwi3RT5fFzqbkr6joyc5FmiOlX4p-Ge2UXud1nP3B58DOPRUjtb2dfBrTY_ags0OiJzfzlH1__-7i7GN5_uXDp7O352VbKalKqrXTzgonqLEciDteuxYcKNFR7Rqn665FR0JYp0SjQGGDWGPddbwDTeKUvTn67pZmJNfSNOdXzC760ca9CdabPzeT781luDICFeSsssGLG4MYfiyUZjP61NIw2InCkoxSMsfMJWTy5T9JBC2kkABVRp__hW7DEqcchMFKVkJABSJT8ki1MaQUqbs7G8Ec-ja3fZtD3-bYd5Y9-_3lO9FtwRnQR-DaD7T_L1Nz8fmrrLkSPwFarL1Q</recordid><startdate>201108</startdate><enddate>201108</enddate><creator>Nelson, Michael D.</creator><creator>Haykowsky, Mark J.</creator><creator>Stickland, Michael K.</creator><creator>Altamirano‐Diaz, Luis A.</creator><creator>Willie, Christopher K.</creator><creator>Smith, Kurt J.</creator><creator>Petersen, Stewart R.</creator><creator>Ainslie, Philip N.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><general>Blackwell Science Inc</general><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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201108</creationdate><title>Reductions in cerebral blood flow during passive heat stress in humans: partitioning the mechanisms</title><author>Nelson, Michael D. ; Haykowsky, Mark J. ; Stickland, Michael K. ; Altamirano‐Diaz, Luis A. ; Willie, Christopher K. ; Smith, Kurt J. ; Petersen, Stewart R. ; Ainslie, Philip N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5848-e69d9da3d3eba20e2d26dc0d083fe6dbd96fc1de33ad83b8081b11616ff2f09e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adult</topic><topic>Blood Flow Velocity - physiology</topic><topic>Blood Pressure - physiology</topic><topic>Body Temperature - physiology</topic><topic>Cerebrovascular Circulation - physiology</topic><topic>Heart Rate - physiology</topic><topic>Heat Stress Disorders - physiopathology</topic><topic>Heat Stress Disorders - prevention & control</topic><topic>Heat-Shock Response - physiology</topic><topic>Humans</topic><topic>Indexing in process</topic><topic>Integrative</topic><topic>Male</topic><topic>Severity of Illness Index</topic><topic>Stroke Volume - physiology</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nelson, Michael D.</creatorcontrib><creatorcontrib>Haykowsky, Mark J.</creatorcontrib><creatorcontrib>Stickland, Michael K.</creatorcontrib><creatorcontrib>Altamirano‐Diaz, Luis A.</creatorcontrib><creatorcontrib>Willie, Christopher K.</creatorcontrib><creatorcontrib>Smith, Kurt J.</creatorcontrib><creatorcontrib>Petersen, Stewart R.</creatorcontrib><creatorcontrib>Ainslie, Philip N.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nelson, Michael D.</au><au>Haykowsky, Mark J.</au><au>Stickland, Michael K.</au><au>Altamirano‐Diaz, Luis A.</au><au>Willie, Christopher K.</au><au>Smith, Kurt J.</au><au>Petersen, Stewart R.</au><au>Ainslie, Philip N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reductions in cerebral blood flow during passive heat stress in humans: partitioning the mechanisms</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2011-08</date><risdate>2011</risdate><volume>589</volume><issue>16</issue><spage>4053</spage><epage>4064</epage><pages>4053-4064</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><coden>JPHYA7</coden><abstract>Non‐technical summary Heat stress reduces brain blood flow and impairs orthostatic tolerance. Brain blood flow is largely controlled by the partial pressure of arterial . Indeed, hyperthermia‐induced over‐breathing and related reductions in arterial account for ∼50% of the reduction in brain blood flow. This investigation tested the unique hypothesis that the distribution of cardiac output during heat stress (challenged by thermoregulatory increases in skin blood flow and sweat loss) contributes to the remaining 50%. We show that cardiac output is not related to brain blood flow, but rather arterial plays a much larger role than previously suggested. These findings help us understand the mechanisms relating heat stress with an increased likelihood of fainting, and are also relevant to pathological conditions that are accompanied by elevations in body temperature.
Cerebral blood flow (CBF) is reduced during passive heat stress, with 50% of this reduction associated with hyperventilatory‐induced hypocapnia and subsequent cerebral vasoconstriction. It remains unknown, however, what other factors may contribute to the remaining 50%. We tested the hypothesis that the distribution of cardiac output plays an important role in maintaining cerebral perfusion during mild and severe heat stress. Middle cerebral artery and posterior cerebral artery blood flow velocity (MCAv and PCAv; transcranial Doppler) and left ventricular end‐diastolic and end‐systolic volumes (2‐D echocardiography) were measured under conditions of normothermia and mild and severe passive heat stress (core temperature +0.8 ± 0.1°C (Protocol I; n= 10) and 1.8 ± 0.1°C (Protocol II; n= 8) above baseline). Venous return was manipulated by passive tilt table positioning (30 deg head‐down tilt (HDT) and 30 deg head‐up tilt (HUT)). Measurements were made under poikilocapnic and isocapnic conditions. Protocol I consisted of mild heat stress which resulted in small reductions in end‐tidal CO2 (−5.6 ± 3.5%), MCAv/PCAv (−7.3 ± 2.3% and −10.3 ± 2.9%, respectively) and stroke volume (−8.5 ± 4.2%); while end‐diastolic volume was significantly reduced (−16.9 ± 4.0%) and cardiac output augmented (17.2 ± 7.4%). During mild heat stress, CBF was related to left ventricular end‐diastolic volume (MCAv, r2= 0.81; PCAv, r2= 0.83; P < 0.05) and stroke volume (MCAv, r2= 0.38; PCAv, r2= 0.43), but not with cardiac output. Protocol II consisted of severe heat stress which resulted in much greater reductions in end‐tidal CO2 (−87.5 ± 31.5%) and CBF (MCAv, −36.4 ± 6.1%; PCAv, −30.1 ± 4.8%; P < 0.01 for all variables), while end‐diastolic volume and stroke volume decreased to a similar extent as for mild heat stress. Importantly, isocapnia restored MCAv and PCAv back to normothermic baseline. This investigation therefore produced two novel findings: first, that venous return and stroke volume are related to CBF during mild heat stress; and second, that hyperventilatory hypocapnia has a major influence on CBF during severe passive heat stress.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>21690194</pmid><doi>10.1113/jphysiol.2011.212118</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Blood Flow Velocity - physiology Blood Pressure - physiology Body Temperature - physiology Cerebrovascular Circulation - physiology Heart Rate - physiology Heat Stress Disorders - physiopathology Heat Stress Disorders - prevention & control Heat-Shock Response - physiology Humans Indexing in process Integrative Male Severity of Illness Index Stroke Volume - physiology Young Adult |
title | Reductions in cerebral blood flow during passive heat stress in humans: partitioning the mechanisms |
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