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Hypoxemia increases blood-brain barrier permeability during extreme apnea in humans.
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- Additional Information
- Source:
Publisher: SAGE Publications Country of Publication: United States NLM ID: 8112566 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1559-7016 (Electronic) Linking ISSN: 0271678X NLM ISO Abbreviation: J Cereb Blood Flow Metab Subsets: MEDLINE
- Publication Information:
Publication: 2016- : Thousand Oaks, CA : SAGE Publications
Original Publication: New York : Raven Press, c1981-
- Subject Terms:
- Abstract:
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.
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- Contributed Indexing:
Keywords: Hypoxia; blood-brain barrier; cerebral blood flow; hypercapnia; hyperoxia
- Publication Date:
Date Created: 20220121 Date Completed: 20220519 Latest Revision: 20220802
- Publication Date:
20221213
- Accession Number:
PMC9121528
- Accession Number:
10.1177/0271678X221075967
- Accession Number:
35061562
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