Protection of the brain from hypoxia: A review

Ping, F. C.; Jenkins, Leonard C.

doi:10.1007/bf03007408

Cited by 17 publications

(4 citation statements)

References 21 publications

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“…Hypoxia is a pathophysiological condition whereby cells or tissues are deprived of oxygen. Hypoxia could be the result of cardiac arrest, carbon dioxide poisoning, suffocation or high altitudes where atmospheric O 2 concentrations are low (Banchero 1987, Ping andJenkins 1978). During acute hypoxia, an insufficient oxygen supply could lead to lactic acid production and accumulation, and prolonged hypoxia could lead to cell death (Kubasiak et al 2002).…”

Section: Introductionmentioning

confidence: 99%

The use of microelectrode array (MEA) to study the protective effects of potassium channel openers on metabolically compromised HL-1 cardiomyocytes

Law

Yeung

Hofmann³

et al. 2009

Physiol. Meas.

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The microelectrode array (MEA) was used to evaluate the cardioprotective effects of adenosine triphosphate sensitive potassium (K(ATP)) channel activation using potassium channel openers (KCOs) on HL-1 cardiomyocytes subjected to acute chemically induced metabolic inhibition. Beat frequency and extracellular action potential (exAP) amplitude were measured in the presence of metabolic inhibitors (sodium azide (NaN(3)) or 2-deoxyglucose (2-DG)) or KCOs (pinacidil (PIN, a cyanoguanidine derivative, activates sarcolemmal K(ATP) channels) or SDZ PCO400 (SDZ, a benzopyran derivative, activates mitochondrial K(ATP) channels)). The protective effects of these KCOs on metabolically inhibited HL-1 cells were subsequently investigated. Signal shapes indicated that NaN(3) and 2-DG reduced the rate of the sodium (Na(+)) influx signal as reflected by a reduction in beat frequency. PIN and SDZ appeared to reduce both rate of depolarization and extent of the Na(+) influx signals. Pre-treating cardiomyocytes with PIN (0.1 mM), but not SDZ, prevented the reduction of beat frequency associated with NaN(3)- or 2-DG-induced metabolic inhibition. The exAP amplitude was not affected by either KCO. The cardioprotective effect of PIN relative to SDZ may be due to the opening of different K(ATP) channels. This metabolic inhibition model on the MEA may provide a stable platform for the study of cardiac pathophysiology in the future.

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Section: Introductionmentioning

confidence: 99%

The use of microelectrode array (MEA) to study the protective effects of potassium channel openers on metabolically compromised HL-1 cardiomyocytes

Law

Yeung

Hofmann³

et al. 2009

Physiol. Meas.

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“…The brain is the most sensitive organ to hypoxia in mammals and vital activity within the brain is mainly dependent on the energy provided by the aerobic oxidation of glucose. Therefore, irreversible injury is induced under a long-time hypoxic environment [ 28 , 29 ]. Thrombolytic therapy and mechanical recanalization are effective methods for blood re-supply after ischemia.…”

Section: Discussionmentioning

confidence: 99%

Agomelatine prevents macrophage infiltration and brain endothelial cell damage in a stroke mouse model

Cao

Wang

et al. 2021

Aging

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Background and purpose: Ischemic/reperfusions are regarded as the clinical consensus for stroke treatment, which results in secondary injury of brain tissues. Increased blood-brain barrier (BBB) permeability and infiltration of inflammatory cells are responsible for the ischemic/reperfusion injury. In the present study, we aimed to investigate the effects of Agomelatine on brain ischemic/reperfusions injury and the underlying mechanism. Methods: MCAO model was established in mice. The expressions of CD68 and claudin-5 in the cerebral cortex were determined using an immunofluorescence assay. Brain permeability was evaluated using Evans blue staining assay. A two-chamber and two-cell trans-well assay was used to detect the migration ability of macrophages through endothelial cells. The expression levels of claudin-5 and MCP-1 in the endothelial cells were determined using qRT-PCR and ELISA. Results: CD68 was found to be up-regulated in the cerebral cortex of MCAO mice but was down-regulated by treatment with Agomelatine. The expression level of down-regulated claudin-5 in the cerebral cortex of MCAO mice was significantly suppressed by Agomelatine. Deeper staining of Evans blue was found in the MCAO group, which was however faded significantly in the Agomelatine treated MCAO mice. The migrated macrophages were significantly increased by hypoxia incubation but were greatly suppressed by the introduction of Agomelatine. The down-regulated claudin-5 by hypoxic incubation in endothelial cells was up-regulated by treatment with Agomelatine. Furthermore, the increased expression of MCP-1 in endothelial cells under hypoxic conditions was significantly inhibited by Agomelatine. Conclusion: Agomelatine prevents macrophage infiltration and brain endothelial cell damage in a stroke mouse model.

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“…Hypoxia also depressed auditory responses in non-mammals, even the crucian carp that is anoxia-resistant (Ping and Jenkins, 1978;Weber, 2016)). Hypoxia was simply produced by stopping water flowing over the gills for up to 20 minutes.…”

Section: Brainstem Responses To Vibration Of the Tympanic Membrane Ar...mentioning

confidence: 99%

Responses of thein vitroturtle brain to visual and auditory stimuli during severe hypoxia

Ariel¹,

Ahuja²,

Warren³

2022

Preprint

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North American pond turtles (Emydidae) are renowned for their ability to survive extreme hypoxia and anoxia, which enables several species to overwinter in ice-locked, anoxic freshwater ponds and bogs for months. Centrally important for surviving these conditions is a profound metabolic suppression, which enables ATP demands to be met entirely with glycolysis. Despite this, turtles have occasionally been observed exploring their natural and laboratory environments while anoxic and can still respond to sensory stimuli. To better understand whether anoxia limits a special sensory function, we recorded evoked potentials in a reduced brain preparation, in vitro, that was perfused with severely hypoxic artificial cerebral spinal fluid (aCSF). For recordings of visual responses, an LED light was flashed onto retinal eyecups while evoked potentials were recorded from the retina or the optic tectum. For recordings of auditory responses, a piezo motor-controlled glass actuator vibrated the tympanic membrane while evoked potentials were recorded from the cochlear nuclei. We found that visual responses decreased even with moderately hypoxic perfusate (aCSF Po2 = 30-60 torr) and completely abolished under severe hypoxia. In contrast, the evoked response within the cochlear nuclei was unattenuated with severe hypoxia (aCSF Po2 < 20 torr). These data provide further support that pond turtles have a limited ability to sense visual information in their environment even while moderately hypoxic, but that auditory input may become a principal avenue of sensory perception during extreme diving in this species.

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Protection of the brain from hypoxia: A review

Cited by 17 publications

References 21 publications

The use of microelectrode array (MEA) to study the protective effects of potassium channel openers on metabolically compromised HL-1 cardiomyocytes

The use of microelectrode array (MEA) to study the protective effects of potassium channel openers on metabolically compromised HL-1 cardiomyocytes

Agomelatine prevents macrophage infiltration and brain endothelial cell damage in a stroke mouse model

Responses of thein vitroturtle brain to visual and auditory stimuli during severe hypoxia

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