Regional Cerebral Pulsatile Hemodynamics During Isocapnic and Poikilocapnic Hyperthermia

Hyperthermia reduces cerebral blood flow, but its impact on pulsatile hemodynamic forces is unknown. Thus, the objective of this secondary analysis was to assess cerebrovascular hemodynamic buffering (damping factor; DFi) during poikilocapnic (HT) and isocapnic (HT-C) hyperthermia. We hypothesized that HT would reduce posterior and anterior DFi, while HT-C would attenuate the reduction in DFi by limiting decreases in flow and increases in resistance. Ten healthy males were passively heated +2 °C from normothermia (BL). Mean arterial pressure was collected using an intra-radial catheter. Blood flow through the extracranial internal carotid artery (ICA) and vertebral artery (VA) was measured using vascular duplex ultrasound. Blood velocity through the middle cerebral artery (MCA) and the posterior cerebral artery (PCA) was measured using transcranial Doppler (TCD) ultrasound. DFi was calculated as the ratio of proximal to distal pulsatility index (PI): Anterior DFi = PI ICA / PI MCA ; Posterior DFi = PI VA / PI PCA . Mean arterial pressure decreased from BL (112±6.0 mmHg) during HT (96±9.7 mmHg, p =<0.001) and HT-C (99±9.6 mmHg, p =<0.001). Intravenous jugular pressure increased from BL (7.0±3.2 mmHg) during HT (8.3±3.0 mmHg, p =0.019) and HT-C (10.3±3.0, p =<0.001). Anterior PI increased in both ICA and MCA from BL (1.0±0.2 a.u; 0.8±0.2 a.u, respectively) during HT (1.6±0.4 a.u; 1.4±0.3 a.u; both p=<0.001), but only PI MCA increased from BL during HT-C (1.1±0.2 a.u, p=0.003). Both ICA and MCA PI HT-C (1.2±0.2 a.u; 1.1±0.2 a.u) was lower than HT (1.6±0.4 a.u; 1.4±0.3 a.u), p =0.001. Posterior PI increased in both the VA and PCA from BL (1.4±0.6 a.u; 0.8±0.2 a.u, respectively) during HT (2.3±0.5; 1.7±0.5 a.u, p =<0.001), but only PI VA increased from BL during HT-C (1.8±0.5 a.u; p =0.003). Both HT PI VA and PCA values were greater than HT-C (1.8±0.5 a.u [ p =<0.001]; 1.0±0.2 a.u [ p =0.006]). BL Anterior DFi (1.3±0.1 a.u) decreased in both HT (1.1±0.2 a.u; p =0.007) and HT-C (1.1±0.2 a.u; p =0.021). Posterior DFi did not change, p =0.116. BL CVC MCA (1.8±0.4 mmHg.ml.min -1 ) increased during HT (2.4±0.5 mmHg.ml.min -1 ; p = <0.001). Irrespective of P a CO 2 clamping, both hyperthermic conditions reduced anterior DFi, suggesting other mechanisms (i.e., intracranial pressure or myogenic tone) are responsible for cerebrovascular hemodynamic buffering. Furthermore, because posterior DFi responses were not observed, preferential buffering of the posterior cerebral circulation protects against deleterious pulsatile hemodynamic forces caused by hyperthermia. NSERC This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.