Abstract
We investigated that the effects of hypercapnia-induced elevations in cerebral perfusion during a heat stress on global cerebrovascular responses to an orthostatic challenge. Seven volunteers completed a progressive lower-body negative pressure (LBNP) challenge to presyncope during heat stress, with or without breathing a hypercapnic gas mixture. Administration of the hypercapnic gas mixture increased the partial pressure of end-tidal CO2 greater than pre-heat stress alone, and increased both internal carotid artery (ICA) and vertebral artery (VA) blood flows (P < 0.05). During LBNP, both ICA and VA blood flows with the hypercapnic gas mixture remained elevated relative to the control trial (P < 0.05). However, at the end of LBNP due to pre-syncopal symptoms, both ICA and VA blood flows decreased to similar levels between trials. These findings suggest that hypercapnia-induced cerebral vasodilation is insufficient to maintain cerebral perfusion at the end of LBNP due to pre-syncope in either the anterior or posterior vascular beds.
Highlights
Passive heat stress reduces orthostatic tolerance [1, 2], but the physiological mechanism(s) responsible for this occurrence remains debatable
The main observations of this study are: (1) despite an increase in both vertebral artery (VA) and internal carotid artery (ICA) blood flows via an inhaling a hypercapnic gas mixture while heat stressed, lower body negative pressure (LBNP) tolerance was not improved; (2) there was no regional difference in the magnitude of the relative reduction in cerebral perfusion between ICA and VA vessels during LBNP for either the also not different between trials (Air) and CO2 trials; (3) at the end of LBNP, both ICA and VA blood flows decreased below the normothermic baseline values regardless of the inhaled gas
Under the imposed combined stresses, hypercapnia-induced increases in cerebral blood flow, due to cerebral vasodilation, is apparently overridden by reductions in perfusion pressure and/or accompanying cerebral vasoconstriction resulting in global decreases in cerebral blood flow. These findings suggest that regional cerebral perfusion cannot be maintained during combined heat and orthostatic stresses despite cerebral blood flow being elevated via the inhalation of a hypercapnic gas mixture
Summary
Passive heat stress reduces orthostatic tolerance [1, 2], but the physiological mechanism(s) responsible for this occurrence remains debatable. Head-up tilt or lower body negative pressure (LBNP) are often used to investigate physiological responses to orthostatic-induced fluid shifts in humans [4]. Hyperthermia associated with passive heat stress induces hyperventilation and associated hypocapnia-induced reductions in cerebral perfusion [5, 6]. Such hyperthermia-induced cerebral hypoperfusion may contribute to heat-induced reductions in orthostatic intolerance [2, 5]. Since cerebral perfusion can be modulated through changes in arterial carbon dioxide tension (PaCO2) [7], it may be that heat-induced orthostatic
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