K ATP channels modulate cerebral blood flow and oxygen delivery during isocapnic hypoxia in humans.

Autor: Rocha MP; Laboratory of Exercise Sciences, Department of Physiology and Pharmacology, Fluminense Federal University, RJ, Brazil., Campos MO; Laboratory of Exercise Sciences, Department of Physiology and Pharmacology, Fluminense Federal University, RJ, Brazil., Mattos JD; Laboratory of Exercise Sciences, Department of Physiology and Pharmacology, Fluminense Federal University, RJ, Brazil., Mansur DE; Laboratory of Exercise Sciences, Department of Physiology and Pharmacology, Fluminense Federal University, RJ, Brazil., Rocha HNM; Laboratory of Exercise Sciences, Department of Physiology and Pharmacology, Fluminense Federal University, RJ, Brazil., Secher NH; Department of Anaesthesia, The Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen, Denmark., Nóbrega ACL; Laboratory of Exercise Sciences, Department of Physiology and Pharmacology, Fluminense Federal University, RJ, Brazil., Fernandes IA; NeuroV̇ASQ̇-Integrative Physiology Laboratory, Faculty of Physical Education, University of Brasília, Brazil.
Jazyk: angličtina
Zdroj: The Journal of physiology [J Physiol] 2020 Aug; Vol. 598 (16), pp. 3343-3356. Date of Electronic Publication: 2020 Jun 12.
DOI: 10.1113/JP279751
Abstrakt: Key Points: ATP-sensitive K + (K ATP ) channels mediate hypoxia-induced cerebral vasodilatation and hyperperfusion in animals. We tested whether K ATP channels blockade affects the increase in human cerebral blood flow (CBF) and the maintenance of oxygen delivery (CDO 2 ) during hypoxia. Hypoxia-induced increases in the anterior circulation and total cerebral perfusion were attenuated under K ATP channels blockade affecting the relative changes of brain oxygen delivery. Therefore, in humans, K ATP channels activation modulates the vascular tone in the anterior circulation of the brain, contributing to CBF and CDO 2 responses to hypoxia.
Abstract: ATP-sensitive K + (K ATP ) channels mediate hypoxia-induced cerebral vasodilatation and hyperperfusion in animals. We tested whether K ATP channels blockade affects the increase in cerebral blood flow (CBF) and the maintenance of oxygen delivery (CDO 2 ) during hypoxia in humans. Nine healthy men were exposed to 5-min trials of normoxia and isocapnic hypoxia (IHX, 10% O 2 ) before (BGB) and 3 h after glibenclamide ingestion (AGB). Mean arterial pressure (MAP), arterial saturation ( S a O 2 ), partial pressure of oxygen ( P a O 2 ) and carbon dioxide ( P aC O 2 ), internal carotid artery blood flow (ICABF), vertebral artery blood flow (VABF), total (t)CBF (Doppler ultrasound) and CDO 2 were quantified during the trials. IHX provoked similar reductions in S a O 2 and P a O 2 , while MAP was not affected by oxygen desaturation or K ATP blockade. A smaller increase in ICABF (ΔBGB: 36 ± 23 vs. ΔAGB 11 ± 18%, p = 0.019) but not in VABF (∆BGB 26 ± 21 vs. ∆AGB 27 ± 27%, p = 0.893) was observed during the hypoxic trial under K ATP channels blockade. Thus, IHX-induced increases in tCBF (∆BGB 32 ± 19 vs. ∆AGB 14 ± 13%, p = 0.012) and CDO 2 relative changes (∆BGB 7 ± 13 vs. ∆AGB -6 ± 14%, p = 0.048) were attenuated during the AGB hypoxic trial. In a separate protocol, 6 healthy men (5 from protocol 1) underwent a 5-min exposure to normoxia and IHX before and 3 h after placebo (5 mg of cornstarch) ingestion. IHX reduced S a O 2 and P a O 2 , but placebo did not affect the ICABF, VABF, tCBF, or CDO 2 responses. Therefore, in humans, K ATP channels activation modulates vascular tone in the anterior rather than the posterior circulation of the brain, contributing to tCBF and CDO 2 responses to hypoxia.
(© 2020 The Authors. The Journal of Physiology © 2020 The Physiological Society.)
Databáze: MEDLINE
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