Utilisateur:JackBortone/Research/Topics/Hypoxia

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Hypoxia-induced hibernation

Introduction

Abstract 

Hypoxia-induced hibernation is ATP-dependent and requires nitric oxide (NO) production to cause cellular damage in hypoxic conditions: By itself hypoxia requires nitric oxide (NO) presence to activate hypoxia-inducible gene factor (HIF) and trigger hypoxic hibernation state. [1]

"Thus, the definition of chronic hypoxia to describe constantly low oxygen saturation levels warrants comment. Some studies describing chronic hypoxia involved patients that were not hypoxaemic based on pulse oxymetry.": See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5619525/

In summary intermittent hypoxic training with a face cover is a highly dysfunctional way to control the respiratory rate of humans by decreasing oxygen availability in tissues thereby inducing a state of hypoxia-mediated hibernation while lowering glucose metabolic rate in conscious subjects. [2]

Secondly, hypoxic hibernation training in humans may decrease oxygen consumption and may compromise sympathetic nerve activity (SNA) and the noradrenergic (arousal) system, a serious risk factor in the pathogenesis of cardiovascular diseases including hyperglycemia and hypertension. [3]

Mechanism

In summary, hypoxia-mediated noradrenergic dysregulation is caused by increased amygdala-striatum reactivity altering the dopamine-noradrenaline response following chronic episodes of mild and intermittent hypoxia (IH), independently of pulse oxymetry status. [4]

Metabolic changes associated to hypoxia-mediated hypometabolism

Hypoxia-induced changes to noradrenergic signaling may activate the sympathetic nervous system thereby lowering cerebral blood glucose levels in the midbrain region (striatum and hippocampus) thus causing memory impairment in cognitive/verbal processing. [1]

Secondly, the upregulation of cerebral blood flow in the striatum caused by hypoxia-induced sympathetic activity (noradrenaline) is influenced mostly by nitric oxide (NO)-mediated metabolic changes (ie: SpO2/FiO2) in tissues... [5]

Experimental

Stress-dependent avoidance conditioning

1. Chronic intermittent hypoxia (CIH) may enhances stress-dependent conditioned responses and dopamine expression in the amygdala. [6]

Consequently, stress-induced persistent reuptake in phasic dopamine (D2) activity in the paraventricular thalamus (PVT) may creates a motivational conflict associated to the neurocircuitry of fear extinction learning and addiction. [7]

2. Intermittent hypoxic stress may enhances COVID-19 associated instrumental conditioning by modulating post-synaptic D2R activity.

3. Identify neurocircuitry of active avoidance : NacS, LH, CeA, etc...

4. PVT-NaC : https://www.sciencedirect.com/science/article/pii/S089662731930443X

Paper: https://open-neurosecurity.org/ahnjournal/repository/view/4/

Sepsis-induced vascular microthrombosis and hypoxia

There is also evidences suggesting a link between systemic hypoxia creating a positive feedback loop with thrombus formation in sepsis patients. It would thus be interesting to know how may protein S deficiency promote microthrombosis in this model.

Most likely severe COVID19 thrombosis is a sepsis-induced endotheliopathy (DIT) promoted by positive feedback loop between inflammation and thrombus generation thereby inhibiting protein S and protein C in hypoxic conditions.

Keywords:

ADAMTS13, Protein S, thrombin, sepsis, microthrombosis, hypoxia, endothelial dysfunction

Paper: https://thrombosisjournal.biomedcentral.com/articles/10.1186/s12959-019-0198-4

References

  1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5619525/

    [paper1]

    Cognition and chronic hypoxia in pulmonary diseases

  2. https://pubmed.ncbi.nlm.nih.gov/15044204/

    [paper8]

    Hypoxia causes glucose intolerance in humans

  3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2681331/

    [paper7]

    Effects of acute intermittent hypoxia on glucose metabolism in awake healthy volunteers

  4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2522385/

    [paper3]

    Chronic intermittent hypoxia sensitizes acute hypothalamic-pituitary-adrenal stress reactivity and Fos induction in the rat locus coeruleus in response to subsequent immobilization stress

  5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6188559/

    [paper4]

    Inhibitory Neuron Activity Contributions to Hemodynamic Responses and Metabolic Load Examined Using an Inhibitory Optogenetic Mouse Model

  6. http://learnmem.cshlp.org/content/20/8/446.full.html

    [paper11]

    Active vs. reactive threat responding is associated with differential c-Fos expression in specific regions of amygdala and prefrontal cortex

  7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6975287/

    [paper9]

    Paraventricular Thalamus Activity during Motivational Conflict Highlights the Nucleus as a Potential Constituent in the Neurocircuitry of Addiction

  8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3063979/

    [paper2]

    Hypoxia regulates cellular metabolism (ATP, nitric oxide)

  9. https://behavioralandbrainfunctions.biomedcentral.com/articles/10.1186/1744-9081-7-17

    [paper5]

    Mental fatigue caused by prolonged cognitive load associated with sympathetic hyperactivity

  10. https://academic.oup.com/jcem/article/98/6/2484/2537184

    [paper6]

    Dysregulation of the Autonomic Nervous System Predicts the Development of the Metabolic Syndrome

  11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5563831

    [paper10]

    The Other Face of the Nucleus Accumbens: Aversion

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