Hypoxemia increases blood-brain barrier permeability during extreme apnea in humans.

Journal Article (Journal Article)

Voluntary asphyxia imposed by static apnea challenges blood-brain barrier (BBB) integrity in humans through transient extremes of hypertension, hypoxemia and hypercapnia. In the present study, ten ultra-elite breath-hold divers performed two maximal dry apneas preceded by normoxic normoventilation (NX: severe hypoxemia and hypercapnia) and hyperoxic hyperventilation (HX: absence of hypoxemia with exacerbating hypercapnia) with measurements obtained before and immediately after apnea. Transcerebral exchange of NVU proteins (ELISA, Single Molecule Array) were calculated as the product of global cerebral blood flow (gCBF, duplex ultrasound) and radial arterial to internal jugular venous concentration gradients. Apnea duration increased from 5 m 6 s in NX to 15 m 59 s in HX (P = <0.001) resulting in marked elevations in gCBF and venous S100B, glial fibrillary acidic protein, ubiquitin carboxy-terminal hydrolase-L1 and total tau (all P < 0.05 vs. baseline). This culminated in net cerebral output reflecting mildly increased BBB permeability and increased neuronal-gliovascular reactivity that was more pronounced in NX due to more severe systemic and intracranial hypertension (P < 0.05 vs. HX). These findings identify the hemodynamic stress to which the apneic brain is exposed, highlighting the critical contribution of hypoxemia and not just hypercapnia to BBB disruption.

Full Text

Duke Authors

Cited Authors

  • Bailey, DM; Bain, AR; Hoiland, RL; Barak, OF; Drvis, I; Hirtz, C; Lehmann, S; Marchi, N; Janigro, D; MacLeod, DB; Ainslie, PN; Dujic, Z

Published Date

  • June 2022

Published In

Volume / Issue

  • 42 / 6

Start / End Page

  • 1120 - 1135

PubMed ID

  • 35061562

Pubmed Central ID

  • PMC9121528

Electronic International Standard Serial Number (EISSN)

  • 1559-7016

Digital Object Identifier (DOI)

  • 10.1177/0271678X221075967


  • eng

Conference Location

  • United States