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

Abstract

CG. Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stress. J Appl Physiol 104: 976-981, 2008. First published January 24, 2008 doi:10.1152/japplphysiol.01040.2007.-This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO2 (PETCO 2 ). Nine healthy subjects (4 men and 5 women), each dressed in a water-perfused suit, underwent normoxic hypocapnic hyperventilation (decrease PETCO 2 ϳ20 Torr) and normoxic hypercapnic (increase in PETCO 2 ϳ9 Torr) 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) and PETCO 2 was used to evaluate cerebrovascular CO2 responsiveness. Passive heat stress increased core temperature (1.1 Ϯ 0.2°C, P Ͻ 0.001) and reduced middle cerebral artery blood velocity by 8 Ϯ 8 cm/s (P ϭ 0.01), reduced CBVC by 0.09 Ϯ 0.09 CBVC units (P ϭ 0.02), and decreased PETCO 2 by 3 Ϯ 4 Torr (P ϭ 0.07), while mean arterial blood pressure was well maintained (P ϭ 0.36). The slope of the CBVC-PET CO 2 relationship to the hypocapnic challenge was not different between normothermia and heat stress conditions (0.009 Ϯ 0.006 vs. 0.009 Ϯ 0.004 CBVC units/Torr, P ϭ 0.63). Similarly, in response to the hypercapnic challenge, the slope of the CBVC-PETCO 2 relationship was not different between normothermia and heat stress conditions (0.028 Ϯ 0.020 vs. 0.023 Ϯ 0.008 CBVC units/Torr, P ϭ 0.31). These results indicate that cerebrovascular CO2 responsiveness, to the prescribed steady-state changes in PETCO 2 , is unchanged during passive heat stress. brain blood flow; hyperthermia; hypocapnia; hypercapnia ORTHOSTATIC TOLERANCE IS REDUCED under heat stress, relative to normothermic, conditions (1,8,19,40,41). Although mechanisms responsible for reduced orthostatic tolerance during heat stress are unclear, they are likely associated with factors that directly or indirectly affect cerebral perfusion pressure, cerebral blood flow, and thus cerebral oxygenation (20, 24,38). Cerebral perfusion is very sensitive to changes in arterial carbon dioxide tension (Pa CO 2 ), such that increases in Pa CO 2 increase cerebral perfusion, whereas decreases in Pa CO 2 decrease cerebral perfusion (16, 36). Previously, our laboratory identified decreases in end-tidal carbon dioxide (PET CO 2 ; surrogate of Pa CO 2 ) of ϳ2 Torr in response to whole body passive heat stress, as well as significant reductions in cerebral perfusion and cerebral vascular conductance (40,41). Decreased cerebral perfusion would theoretically reduce the functional reserve by which cerebral blood flow can decrease further, before the onset of syncopal symptoms.It is unlikely that the relatively small decrease in PET CO 2 (i.e., ϳ2 Torr) in response to passive heat stress is the sole mechanism leading to the observed reduction in cerebral perfusion. However, this assumption is based on ca...

Blood Flow Distribution during Heat Stress: Cerebral and Systemic Blood Flow

“…However, their follow-up study showed that MCAV mean did not return to the baseline level during heat stress (internal temperature increased by 1.41C) even when P ET CO 2 was clamped to the preheating. 11,12 In the present study, we also calculated the relationship between changes in P ET CO 2 and changes in ICA and VA blood flows throughout heat stress, but there was no significant relationship. We did not perform any perturbation to change P ET CO 2 in this study.…”

“…3 In addition, it is well known that heat stress modifies distribution of blood flow toward cutaneous circulation while decreasing renal and splanchnic blood flows by enhanced vasoconstriction. 15,19 Maintained or decreased cerebral blood velocity during heat stress has been reported [10][11][12][20][21][22][23] but the mechanism remains unclear. The present study demonstrated that CBF conductance in MCAV mean , ICA, and VA gradually decreased during whole body heating, whereas CVC forehead and ECA conductance increased by 3 times and 2.5 times from the baseline, respectively.…”

Cerebral Vasomotor Reactivity during Hypo- and Hypercapnia in Sedentary Elderly and Masters Athletes

“…[14][15][16] For these reasons, cerebral CO2 reactivity to hypocapnia (hyperventilation) and hypercapnia (rebreathing) was assessed separately in this study.…”

End-tidal carbon dioxide tension reflects arterial carbon dioxide tension in the heat-stressed human with and without simulated hemorrhage

“…Studies using end-tidal carbon dioxide tension (PET CO 2 ) to estimate Pa CO 2 during passive heat stress (i.e., increase in internal temperature ϳ1.2-1.5°C) suggest that heat stress reduces Pa CO 2 ϳ4 -8 mmHg (3,5,15,26). A potential limitation to these studies is the assumption that PET CO 2 is an accurate surrogate for Pa CO 2 , the latter being the physiologically relevant variable.…”

“…To our knowledge, however, there is no information regarding the relationship of PET CO 2 to Pa CO 2 in individuals with elevated internal temperatures. This information is important because heat stress-induced reductions in Pa CO 2 likely contribute to reductions in cerebral blood flow (3,5,15,26) and ultimately reduced orthostatic tolerance in this thermal condition (4,12,25). Because PET CO 2 is commonly used as an index of Pa CO 2 in heat-stressed individuals (3,5,15,26), it is important to identify the relationship between these variables in this thermal condition.…”