Regional cerebral pulsatile hemodynamics during isocapnic and poikilocapnic hyperthermia in young men

Hyperthermia is known to induce hypocapnia-driven reductions in cerebral blood flow; however, it is unknown if it causes changes in hemodynamic pulsatility that negatively influence cerebrovascular function. This retrospective analysis aimed to assess cerebrovascular hemodynamic pulsatile buffering (damping factor; DFi) during poikilocapnic (HT) and isocapnic (HT-C) hyperthermia. We hypothesized that HT would reduce cerebral DFi, while HT-C would attenuate the reduction in DFi by limiting increases in resistance. Ten healthy males were passively heated +2°C from normothermia (BL). Blood flow through the internal carotid artery (ICA) and vertebral artery (VA) was measured using vascular ultrasound. Blood velocity through the middle cerebral artery (MCA) and the posterior cerebral artery (PCA) was measured using transcranial ultrasound. DFi was calculated as the ratio of proximal to distal pulsatility index (PI): Anterior cerebral DFi = PI_ICA/PI_MCA; Posterior cerebral DFi = PI_VA/PI_PCA. Anterior DFi decreased in both HT (1.08 ± 0.19 a.u; p = 0.007) and HT-C (1.12 ± 0.231 a.u; p = 0.021) conditions from BL values (1.27 ± 0.14 a.u). No changes were observed in posterior DFi, p = 0.116. Irrespective of P_aCO₂ clamping, both hyperthermic conditions reduced anterior DFi, suggesting other mechanisms are responsible for cerebrovascular hemodynamic buffering. Posterior DFi responses were not observed, suggesting preferential buffering of the hyperthermic posterior circulation (VA-PCA).