Journal of Applied Physiology AJP: Lung Cellular and Molecular Physiology
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J Appl Physiol (January 31, 2008). doi:10.1152/japplphysiol.01040.2007
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Submitted on September 28, 2007
Accepted on January 17, 2008

Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stress

David A. Low1, Jonathan Wingo1, David Melvin Keller2, Scott L. Davis2, Rong Zhang2, and Craig G. Crandall2*

1 Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, Texas, United States
2 Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, Texas, United States; Internal Medicine, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd, dallas, California, United States

* To whom correspondence should be addressed. E-mail: craigcrandall{at}texashealth.org.

This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO2 (PETCO2). Nine healthy subjects (4 males and 5 females), each dressed in a water perfused suit, underwent normoxic hypocapnic hyperventilation (decrease PETCO2 ~20 mm Hg) and normoxic hypercapnic (increase in PETCO2 ~9 mm Hg) challenges under normothermic and passive heat stress conditions. The slope of the relationship between calculated cerebrovascular conductance (CBVC; middle cerebral artery blood velocity·mean arterial blood pressure-1) and PETCO2 was used to evaluate cerebrovascular CO2 responsiveness. Passive heat stress increased core temperature (mean ± SD 1.1 ± 0.2 °C, P < 0.001) and reduced middle cerebral artery blood velocity by 8 ± 8 cm·s-1 (P = 0.01), reduced CBVC by 0.09 ± 0.09 CBVC units (P = 0.02), and decreased PETCO2by 3.0 ± 4 mm Hg (P = 0.07), while mean arterial blood pressure was well maintained (P = 0.36). The slope of the CBVC:PETCO2 relationship to the hypocapnic challenge was not different between normothermia and heat stress conditions (0.009 ± 0.006 vs 0.009 ± 0.004 CBVC units·mm Hg-1, respectively, P = 0.63). Similarly, in response to the hypercapnic challenge, the slope of the CBVC:PETCO2 relationship was not different between normothermia and heat stress conditions (0.028 ± 0.020 vs 0.023 ± 0.008 CBVC units·mm Hg-1, respectively, P = 0.36). These results indicate that cerebrovascular CO2 responsiveness, to the prescribed steady-state changes in PETCO2, is unchanged during passive heat stress.




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