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Cerebrovascular responsiveness to steady‐state changes in CO 2 during passive heat stress
Author(s) -
Low David Andrew,
Wingo Jonathan E,
Keller David M,
Kimura Kenichi,
Zhang Rong,
Davis Scott L,
Crandall Craig G
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1311-c
This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady‐state changes in CO 2 . Nine subjects underwent normoxic hypocapnic hyperventilation [decrease end‐tidal CO 2 (P ETCO2 ) ~20 mmHg] and normoxic hypercapnia (increase P ETCO2 ~9 mmHg via breathing 5% CO 2 ) under normothermic (NT) and passive heat stress (HS; increase internal temperature ~1 °C via water‐perfused suit) conditions. The slope of the relationship between calculated cerebrovascular conductance [CBVC; middle cerebral artery blood velocity (MCAV mean )/mean arterial blood pressure (MAP)] and P ETCO2 was used as an index of cerebral CO 2 responsiveness. Passive heat stress reduced MCAV mean (−8 ± 3 cm.sec −1 , P < 0.05), CBVC (−0.09 ± 0.03 CBVC units, P < 0.05), and P ETCO2 (−3.00 ± 1.46 mmHg, P = 0.07), while MAP was unchanged. Relative to normothermia, passive heat stress did not change the slope of the CBVC:P ETCO2 relationship in either the hypocapnic (NT 0.009 ± 0.002 vs HS 0.009 ± 0.001 CBVC units.mmHg −1 , respectively, P > 0.05) or hypercapnic ranges (NT 0.028 ± 0.005 vs HS 0.023 ± 0.003 CBVC units.mmHg −1 , respectively, P > 0.05). These results indicate that cerebrovascular CO 2 responsiveness, to the prescribed steady‐state changes in P ETCO2 , is unchanged during passive heat stress. This research project was funded by grants from the National Heart, Lung and Blood Institute (HL‐61388, HL‐67422, HL‐84072).