The effects of reduced end‐tidal carbon dioxide tension on cerebral blood flow during heat stress
- 30 July 2009
- journal article
- research article
- Published by Wiley in The Journal of Physiology
- Vol. 587 (15), 3921-3927
- https://doi.org/10.1113/jphysiol.2009.172023
Abstract
Passive heat stress reduces arterial carbon dioxide partial pressure (P(aCO2)) as reflected by 3 to 5 Torr reductions in end-tidal carbon dioxide tension (P(ETCO2)). Heat stress also reduces cerebrovascular conductance (CBVC) by up to 30%. While is a strong regulator of CBVC, it is unlikely that the relatively small change in during heating is solely responsible for the reductions in CBVC. This study tested the hypothesis that P(aCO2), referenced by P(ETCO2), is not the sole mechanism for reductions in CBVC during heat stress. Mean arterial blood pressure (MAP), P(ETCO2), middle cerebral artery blood velocity (MCA V(mean)), and calculated CBVC (MCA V(mean)/MAP) were assessed in seven healthy individuals, during three separate conditions performed sequentially: (1) normothemia, (2) control passive heat stress and (3) passive heat stress with P(ETCO2) clamped at the normothermic level (using a computer-controlled sequential gas delivery breathing circuit). MAP was similar in the three thermal conditions (P = 0.55). Control heat stress increased internal temperature approximately 1.3 degrees C, which resulted in decreases in P(ETCO2), MCA V(mean) and calculated CBVC (P < 0.001 for all variables). During heat stress + clamp conditions internal temperature remained similar to that during the control heat stress condition (P = 0.31). Heat stress + clamp successfully restored to the normothermic level (P = 0.99) and increased MCA V(mean) (P = 0.002) and CBVC (P = 0.008) relative to control heat stress. Despite restoration of P(ETCO2), MCA V(mean) (P = 0.005) and CBVC (P = 0.03) remained reduced relative to normothermia. These results indicate that heat stress-induced reductions in , as referenced by P(ETCO2), contribute to the decrease in MCA V(mean) and CBVC; however, other factors (e.g. perhaps elevated sympathetic nerve activity) are also involved in mediating this response.Keywords
This publication has 45 references indexed in Scilit:
- Acute volume expansion preserves orthostatic tolerance during whole‐body heat stress in humansThe Journal of Physiology, 2009
- Non‐invasive prospective targeting of arterial P in subjects at restThe Journal of Physiology, 2008
- Autonomic Neural Control of the Cerebral VasculatureStroke, 2008
- Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stressJournal of Applied Physiology, 2008
- Effects of passive heating on central blood volume and ventricular dimensions in humansThe Journal of Physiology, 2008
- Prospective targeting and control of end‐tidal CO2 and O2 concentrationsThe Journal of Physiology, 2007
- Heat stress reduces cerebral blood velocity and markedly impairs orthostatic tolerance in humansAmerican Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2006
- Heat stress enhances arterial baroreflex control of muscle sympathetic nerve activity via increased sensitivity of burst gating, not burst area, in humansThe Journal of Physiology, 2006
- A comparison of transcranial Doppler and cerebral blood flow studies to assess cerebral vasoreactivity.Stroke, 1992
- Transcranial Doppler measurement of middle cerebral artery blood flow velocity: a validation study.Stroke, 1986