Premium
Human cerebrovascular responses to diving are not related to facial cooling
Author(s) -
AlSalahi Sultan E.,
Braz Igor D.,
Ahmed Amar,
Junejo Rehan T.,
Fisher James P.
Publication year - 2020
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep087529
Subject(s) - cerebral blood flow , medicine , anesthesia , middle cerebral artery , blood flow , stimulation , facial nerve , cerebral arteries , cardiology , surgery , ischemia
New FindingsWhat is the central question of this study? Does facial cooling‐mediated stimulation of cutaneous trigeminal afferents associated with the diving response increase cerebral blood flow or are factors associated with breath‐holding (e.g. arterial carbon dioxide accumulation, pressor response) more important in humans?What is the main finding and its importance? Physiological factors associated with breath‐holding such as arterial carbon dioxide accumulation and the pressor response, but not facial cooling (trigeminal nerve stimulation), make the predominant contribution to diving response‐mediated increases in cerebral blood flow in humans.Abstract Diving evokes a pattern of physiological responses purported to preserve oxygenated blood delivery to vital organs such as the brain. We sought to uncouple the effects of trigeminal nerve stimulation on cerebral blood flow (CBF) from other modifiers associated with the diving response, such as apnoea and changes in arterial carbon dioxide tension. Thirty‐seven young healthy individuals participated in separate trials of facial cooling (FC, 3 min) and cold pressor test (CPT, 3 min) under poikilocapnic (Protocol 1) and isocapnic conditions (Protocol 2), facial cooling while either performing a breath‐hold (FC +BH) or breathing spontaneously for a matched duration (FC −BH) (Protocol 3), and BH during facial cooling (BH +FC) or without facial cooling (BH −FC) (Protocol 4). Under poikilocapnic conditions neither facial cooling nor CPT evoked a change in middle cerebral artery blood flow velocity (MCA v mean ; transcranial Doppler) ( P > 0.05 vs . baseline). Under isocapnic conditions, facial cooling did not change MCA v mean ( P > 0.05), whereas CPT increased MCA v mean by 13% ( P < 0.05). Facial cooling with a concurrent BH markedly increased MCA v mean (Δ23%) and internal carotid artery blood flow (ICA Q ; duplex Doppler ultrasound) (Δ26%) ( P < 0.001), but no change in MCA v mean and ICA Q was observed when facial cooling was accompanied by spontaneous breathing ( P > 0.05). Finally, MCA v mean and ICA Q were similarly increased by BH either with or without facial cooling. These findings suggest that physiological factors associated with BH, and not facial cooling (i.e. trigeminal nerve stimulation) per se , make the predominant contribution to increases in CBF during diving in humans.