Impact of acute changes in blood pressure and arterial stiffness on cerebral pulsatile haemodynamics in young and middle‐aged adults

• Published in: Experimental physiology 2021-07, Vol.106 (7), p.1643-1653
• Main Authors: Lefferts, Wesley K., Lefferts, Elizabeth C., Hibner, Brooks A., Smith, Kurt J., Fernhall, Bo
• Format: Article
• Language: English
• Subjects: Adult; arterial stiffness; Blood Flow Velocity - physiology; Blood pressure; Blood Pressure - physiology; Carotid artery; cerebral haemodynamics; Cerebrovascular Circulation - physiology; Female; Hemodynamics; Humans; Middle Aged; pulsatility; Pulse Wave Analysis; Vascular Stiffness - physiology; Velocity; Young Adult; Young adults
• ISSN: 0958-0670; 1469-445X
• DOI: 10.1113/EP089319

New Findings What is the central question of this study? Does cerebrovascular pulsatility respond differently to acute increases in arterial stiffness in middle‐aged compared with young adults? What is the main finding and its importance? Compared with young adults, middle‐aged adults exhibited similar changes in cerebral pulsatile damping despite attenuated changes in carotid diameter and cerebrovascular pulsatility during blood pressure‐dependent, but not blood pressure‐independent, increases in large artery stiffness. Acute manipulation of arterial stiffness through interventions that increase sympathetic activity might provoke cerebral pulsatility and damping and reveal whether cerebrovascular haemodynamics respond differently to transient elevations in arterial stiffness in middle‐aged compared with young adults. We compared cerebral pulsatility and damping in middle‐aged versus young adults during two different sympathetic interventions [cold pressor test (CP) and lower‐body negative pressure (LBNP)] that increase arterial stiffness acutely. Cerebrovascular haemodynamics were assessed in 15 middle‐aged (54 ± 7 years old; 11 female) and 15 sex‐matched young adults (25 ± 4 years old) at rest and during the CP test (4 min, 6.4 ± 0.8°C) and LBNP (6 min, −20 mmHg). Mean blood pressure was measured continuously via finger photoplethysmography. Carotid–femoral pulse wave velocity (cfPWV) and carotid stiffness were measured via tonometry and ultrasound. Blood velocity pulsatility index (PI) was measured at the middle cerebral (MCA) and common carotid artery (CCA) using Doppler, with pulsatile damping calculated as CCA PI divided by MCA PI. Increases in cfPWV were driven by changes in mean pressure during CP but not during LBNP in both groups (P