Cerebral Blood Flow Pulsatility Index is Unchanged during Superimposed Lower‐Body Negative Pressure in Head‐Up Tilt in Anterior and Posterior Cerebral Circulations

Lower body negative pressure (LBNP) chambers can be utilized to experimentally‐elicit reductions in blood pressure, cerebral blood flow (CBF) and associated symptoms of presyncope. There is high between‐individual variability in tolerance to LBNP, however the underlying physiological responses affecting tolerance remains unclear. Pulsatility in CBF may affect LBNP tolerance, as more pulsatile flow may protect the delivery of oxygen to cerebral tissues in hypotension. We aimed to assess the pulsatility index (PI) in anterior and posterior cerebral circulations during LBNP in superimposed head‐up tilt (HUT), where gravitational‐induced blood volume re‐distribution augments volume unloading during LBNP. We recruited and included 12 healthy male participants, and instrumented them in a custom‐build integrated 45° HUT‐LBNP chamber. Participants were instrumented for heart rate (HR; ECG), end‐tidal CO 2 (P ET CO 2 ; mouthpiece and gas analyzer),beat‐by‐beat mean arterial pressure (MAP; finometer), and middle and posterior cerebral artery velocity (MCAv, PCAv; transcranial Doppler ultrasound). All measures were recorded during baseline (BL) and during ‐50 mmHg LBNP exposure up to a maximum of 10‐minutes (600s). Presyncope was defined as a 30% reduction in systolic blood pressure (i.e., investigator stop) or onset subjective symptoms (i.e., participant stop). We quantified all variables as a 30‐sec mean bin during BL and the final 30‐sec of LBNP prior to presyncope. MAP, MCAv and PCAv PI was calculated as systolic‐diastolic/mean. LBNP tolerance time was 480.9±134.3 sec. HR increased from 72.3±10.3 (BL) to 103.0±18.2 bpm (P<0.01) during LBNP, suggesting a baroreflex response, and P ET CO 2 was reduced from 32.0±2.9 (BL) to 28.7±2.9 Torr (P<0.01) during LBNP, suggesting mild hyperventilation. MAP decreased from 84.8±11.3 (BL) to 76.2±14.7 mmHg (P<0.01) during LBNP, with associated reductions in mean MCAv from 52.1±15.0 to 44.3±14.5 cm/s (P<0.01), and mean PCAv from 35.5±12.6 to 29.0±9.9 cm/s (P<0.01) during LBNP. MAP PI was reduced from 0.76±0.2 to 0.59±0.02 (P<0.01) during LBNP. However, MCAv and PCAv PI were unchanged during LBNP (P=0.6 and P=0.9, respectively). Our results suggest that although MAP and MAP PI were both reduced during LBNP at pre‐syncope, with associated reductions in mean MCAv and PCAv, MCAv and PCAv PI remained stable with LBNP in HUT. These findings suggest that PI in CBF variables at the cardiac frequency are not related to LBNP tolerance in healthy men.