We investigated 1) the regional distribution of cerebral blood flow (CBF), 2) the influence of end-tidal Pco2 (PetCO2) on CBF, and 3) the potential for an extracranial blood "steal" from the anterior brain region during passive hyperthermia. Nineteen (13 male) volunteers underwent supine passive heating until a steady-state esophageal temperature of 2°C above resting was established. Measurements were obtained 1) during normothermia (Normo), 2) during poikilocapnic hyperthermia (Hyper), and 3) during hyperthermia with PetCO2 and end-tidal Po2 clamped to Normo levels (Hyper-clamp). Blood flow in the internal carotid (Qica), vertebral (QVA), and external carotid (Qeca) arteries (Duplex ultrasound), blood velocity of the middle cerebral (MCAv) and posterior cerebral (PCAv) arteries (transcranial Doppler), and cutaneous vascular conductance on the cheek (cheek CVC; Doppler velocimetry) were measured at each stage. During Hyper, PetCO2 was lowered by 7.0 ± 5.2 mmHg, resulting in a reduction in Qica (-18 ± 17%), Qva (-31 ± 21%), MCAv (-22 ± 13%), and PCAv (-18 ± 10%) compared with Normo (P < 0.05). The reduction in QVA was greater than that in QICA (P = 0.017), MCAv (P = 0.047), and PCAv (P = 0.034). Blood flow/velocity was completely restored in each intracranial vessel (ICA, VA, MCA, and PCA) during Hyper-clamp. Despite a ∼250% increase in QECA and a subsequent increase in cheek CVC during Hyper compared with Normo, reductions in QICA were unrelated to changes in QECA. These data provide three novel findings: 1) hyperthermia attenuates QVA to a greater extent than QICA, 2) reductions in CBF during hyperthermia are governed primarily by reductions in arterial Pco2, and 3) increased QECA is unlikely to compromise QICA during hyperthermia.
Keywords: brain blood flow; cerebral blood flow; heat stress; hyperthermia; syncope.