Effect of hyperbaric oxygenation on brain hemodynamics, hemoglobin oxygenation and mitochondrial NADH

Meirovithz, Elhanan; Sonn, Judith; Mayevsky, Avraham

doi:10.1016/j.brainresrev.2007.04.004

Cited by 32 publications

(20 citation statements)

References 40 publications

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“…A longer lasting NADH increase followed in the wake of SD in some studies, coinciding with the post-SD oligemia (50, 185,532). Regardless of the direction of change, the NADH redox shifts were fairly large in magnitude, approaching the decrease induced by hyperbaric hyperoxia or mitochondrial uncouplers, or the increase (e.g., 2-fold) induced by anoxia or inhibitors of mitochondrial respiratory chain, in vivo (187,296,300,301,311,390). Because ouabain significantly slows down the NADH oxidation rate during SD, stimulation of Na ϩ -K ϩ -ATPase is likely to be a significant contributor to the increase in energy consumption (252).…”

Section: B Mitochondrial Redox Statementioning

confidence: 94%

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Ayata

Lauritzen

2015

Physiological Reviews

470

600

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Spreading depression (SD) is a transient wave of near-complete neuronal and glial depolarization associated with massive transmembrane ionic and water shifts. It is evolutionarily conserved in the central nervous systems of a wide variety of species from locust to human. The depolarization spreads slowly at a rate of only millimeters per minute by way of grey matter contiguity, irrespective of functional or vascular divisions, and lasts up to a minute in otherwise normal tissue. As such, SD is a radically different breed of electrophysiological activity compared with everyday neural activity, such as action potentials and synaptic transmission. Seventy years after its discovery by Leão, the mechanisms of SD and its profound metabolic and hemodynamic effects are still debated. What we did learn of consequence, however, is that SD plays a central role in the pathophysiology of a number of diseases including migraine, ischemic stroke, intracranial hemorrhage, and traumatic brain injury. An intriguing overlap among them is that they are all neurovascular disorders. Therefore, the interplay between neurons and vascular elements is critical for our understanding of the impact of this homeostatic breakdown in patients. The challenges of translating experimental data into human pathophysiology notwithstanding, this review provides a detailed account of bidirectional interactions between brain parenchyma and the cerebral vasculature during SD and puts this in the context of neurovascular diseases.

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Section: B Mitochondrial Redox Statementioning

confidence: 94%

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Ayata

Lauritzen

2015

Physiological Reviews

470

600

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“…During hyperbaric hyperoxia at 3 ATA, systemic arterial pO 2 reaches B2000 mm Hg. At partial pressures > 3 ATA, brain concentrations of oxygenated hemoglobin and thus microcirculatory hemoglobin saturation reach a maximum (Meirovithz et al, 2007), the amount of physically dissolved oxygen significantly increases up to 7 mL/100 mL blood, and tissue pO 2 in the brain increases to more than 400 mm Hg (Demchenko et al, 2005;Jamieson and Van den Brenk, 1962). As shown by Demchenko et al (2005), tissue pO 2 values of above 400 mm Hg were reached already at 3 ATA when hyperoxygenation-induced decrease of resting CBF was prevented by acetazolamide application, which slightly elevated the arterial pCO 2 up to 44 mm Hg.…”

Section: During Hyperbaric Hyperoxia Physically Dissolved Oxygen Fulmentioning

confidence: 99%

“…In this study, owing to spontaneous breathing in the hyperbaric chamber, arterial pCO 2 and resting CBF were increased to values comparable with those achieved by Demchenko et al, (2005), suggesting an equally elevated tissue pO 2 of > 400 mm Hg. This increase in tissue O 2 leads to a complete oxidation of cytochrome oxidase type aa3 (Hempel et al, 1977) and of mitochondrial NADH (Meirovithz et al, 2007). During HBO, oxygen consumption during neuronal activation could therefore be matched (3 ATA) or even exceeded (4 ATA) by the amount of physically dissolved oxygen.…”

Section: During Hyperbaric Hyperoxia Physically Dissolved Oxygen Fulmentioning

confidence: 99%

Neurovascular Coupling in Rat Brain Operates Independent of Hemoglobin Deoxygenation

Lindauer

Leithner

Kaasch

et al. 2009

J Cereb Blood Flow Metab

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Recently, a universal, simple, and fail-safe mechanism has been proposed by which cerebral blood flow (CBF) might be coupled to oxygen metabolism during neuronal activation without the need for any tissue-based mechanism. According to this concept, vasodilation occurs by local erythrocytic release of nitric oxide or ATP wherever and whenever hemoglobin is deoxygenated, directly matching oxygen demand and supply in every tissue. For neurovascular coupling in the brain, we present experimental evidence challenging this view by applying an experimental regime operating without deoxy-hemoglobin. Hyperbaric hyperoxygenation (HBO) allowed us to prevent hemoglobin deoxygenation, as the oxygen that was physically dissolved in the tissue was sufficient to support oxidative metabolism. Regional CBF and regional cerebral blood oxygenation were measured using a cranial window preparation in anesthetized rats. Hemodynamic and neuronal responses to electrical forepaw stimulation or cortical spreading depression (CSD) were analyzed under normobaric normoxia and during HBO up to 4 ATA (standard atmospheres absolute). Inconsistent with the proposed mechanism, during HBO, CBF responses to functional activation or CSD were unchanged. Our results show that activation-induced CBF regulation in the brain does not operate through the release of vasoactive mediators on hemoglobin deoxygenation or through a tissue-based oxygen-sensing mechanism.

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“…In the latter, this has been demonstrated in the brain, retina, myocardium, and in skeletal muscle. Vasodilatation in the microcirculation in some tissues has also been reported [11].…”

mentioning

confidence: 96%

Bone and Soft Tissue Blood Flow during Normobaric and Hyperbaric Oxygen Breathing in Healthy Divers

Larsson¹,

Uusijärvi²,

Näslund³

et al. 2014

JBiSE

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Purpose: The study aimed to investigate, using a photoplethysmographic (PPG) technique, how pulsatile blood flow within the patellar bone and skin over the patella reacts to normobaric (NBO) and hyperbaric oxygen breathing (HBO). Methods: Eleven healthy volunteers, breathed air or oxygen. Subjects were blinded to breathing gas. A range of partial pressures of oxygen were administered in 10 minute intervals: 21 kPa, 101 kPa (NBO), 21 kPa, (compression to 280 kPa), 59 kPa, 280 kPa (HBO), 59 kPa, (decompression), and 21 kPa. Changes were measured continuously for each individual. Results: Hyperoxia decreased pulsatile patellar blood flow ~32 resp. 38% and skin blood flow ~36 resp. 42% during the first 2 -3 minutes of NBO resp. HBO. This decrease was normalized within 5 minutes after exposure. The results were similar when switching from air to NBO (101 kPa) and from air at pressure (59 kPa) to HBO (280 kPa). Conclusions: The study shows that pulsatile patellar skin and bone blood flow, decreases significantly as a reaction to oxygen breathing in healthy subjects. The results suggest that a non-invasive PPG technique could be used to monitor blood flow changes in bone during oxygen treatment.

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Effect of hyperbaric oxygenation on brain hemodynamics, hemoglobin oxygenation and mitochondrial NADH

Cited by 32 publications

References 40 publications

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Neurovascular Coupling in Rat Brain Operates Independent of Hemoglobin Deoxygenation

Bone and Soft Tissue Blood Flow during Normobaric and Hyperbaric Oxygen Breathing in Healthy Divers

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