Regional changes in brain blood flow during severe passive hyperthermia: effects of Pa^sub CO2^ and extracranial blood flow

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 (Q...), vertebral (Q...), and external carotid (Q...) 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 Q... (-18 ± 17%), Q... (-31 ± 21%), MCAv (-22 ± 13%), and PCAv (-18 ± 10%) compared with Normo (P < 0.05). The reduction in Q... was greater than that in Q... (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 Q... and a subsequent increase in cheek CVC during Hyper compared with Normo, reductions in Q... were unrelated to changes in Q... These data provide three novel findings: 1) hyperthermia attenuates Q... to a greater extent than Q..., 2) reductions in CBF during hyperthermia are governed primarily by reductions in arterial Pco2, and 3) increased Q... is unlikely to compromise Q... during hyperthermia. (ProQuest: ... denotes formulae/symbols omitted.)