Hypercapnic hypoxia improves cognitive and motor functions of children with cerebral palsy

Kulikov, V. V.; Tregub, Pavel; Parshin, DV; Smirnova, YuV; Смирнов, К. В.

doi:10.1080/01616412.2022.2051130

Cited by 4 publications

(3 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, in a randomized, triple-blind, placebo-controlled study involving 42 cerebral palsy patients with hypertensive manifestations aged 3 to 7 years. After a course of 14-16 20-minute hypercapnic hypoxia sessions, evoked potentials showed a decrease in the peak latency of the P3 component in the test group, a decrease in the central conduction time of impulses by 2.2-2.5 ms during magnetic stimulation, and a decrease in the excitation threshold of the motor cortex by 12-16% depending on lateralization [50].…”

Section: Is the Hypercapnic Acidosis Key To Neuroprotection?mentioning

confidence: 95%

Neuroprotective effect of hypoxic-hypercapnic training. Review

Tolstun,

Kholin

2023

A&L

View full text Add to dashboard Cite

The neuroprotective effects of hypercapnia, especially with hypoxia combined, interested in the context of nerve cells forming protective mechanisms. Hypercapnia not only acts as a potent neuroprotector but also increases tissue tolerance to ischemia and reperfusion. Hypercapnic effects are based on many different mechanisms including energy metabolism modulation, adaptive signaling pathways activation, histological damage reduction, pro-inflammatory factors, angiogenesis activation, and activation of synthetic processes in neurons. The summarized data indicate prospects for further research to better understand the molecular and physiological aspects of neuroprotection during hypercapnia and hypoxia, as well as to determine the conditions under which the best neuroprotective effect is achieved with a subsequent reduction in neurological deficits. __________________________________________________________________________________________ Keywords: hypercapnia, hypoxia, neuroprotection, permissive hypercapnia, ischemia, stroke

show abstract

Section: Is the Hypercapnic Acidosis Key To Neuroprotection?mentioning

confidence: 95%

Neuroprotective effect of hypoxic-hypercapnic training. Review

Tolstun,

Kholin

2023

A&L

View full text Add to dashboard Cite

show abstract

“…Clinical studies have demonstrated the effectiveness of hypercapnic-hypoxic training in the treatment of neurological disorders and diseases. For example, in a randomized triple-blind placebo-controlled study, respiratory training with hypercapnic hypoxia was shown to have a positive effect on the functional state of the nervous system in children with cerebral palsy and can be used as a means to increase the effectiveness of standard therapy for these patients [187]. Additionally, the effectiveness of hypercapnic hypoxia has been demonstrated in the treatment of diabetic polyneuropathy in pediatric patients [188].…”

Section: Future Directions and Potential For Clinical Applicationmentioning

confidence: 99%

Molecular Mechanisms of Neuroprotection after the Intermittent Exposures of Hypercapnic Hypoxia

Tregub,

Kulikov,

Ibrahimli

et al. 2024

IJMS

View full text Add to dashboard Cite

The review introduces the stages of formation and experimental confirmation of the hypothesis regarding the mutual potentiation of neuroprotective effects of hypoxia and hypercapnia during their combined influence (hypercapnic hypoxia). The main focus is on the mechanisms and signaling pathways involved in the formation of ischemic tolerance in the brain during intermittent hypercapnic hypoxia. Importantly, the combined effect of hypoxia and hypercapnia exerts a more pronounced neuroprotective effect compared to their separate application. Some signaling systems are associated with the predominance of the hypoxic stimulus (HIF-1α, A1 receptors), while others (NF-κB, antioxidant activity, inhibition of apoptosis, maintenance of selective blood–brain barrier permeability) are mainly modulated by hypercapnia. Most of the molecular and cellular mechanisms involved in the formation of brain tolerance to ischemia are due to the contribution of both excess carbon dioxide and oxygen deficiency (ATP-dependent potassium channels, chaperones, endoplasmic reticulum stress, mitochondrial metabolism reprogramming). Overall, experimental studies indicate the dominance of hypercapnia in the neuroprotective effect of its combined action with hypoxia. Recent clinical studies have demonstrated the effectiveness of hypercapnic–hypoxic training in the treatment of childhood cerebral palsy and diabetic polyneuropathy in children. Combining hypercapnic hypoxia with pharmacological modulators of neuro/cardio/cytoprotection signaling pathways is likely to be promising for translating experimental research into clinical medicine.

show abstract

“…Hypoxic effects have also been studied on brain tissues especially in cerebral palsy and encephalopathy research (Kim et al, 2012;Novak et al, 2018;Chen et al, 2021;Kulikov et al, 2022). Brain tissues are effective models to assess hypoxia effects because: (1) the tissues' location pass the blood brain barrier, (2)their low regenerative potential allowing apoptosis to be a marker for brain injury, and (3) brain tissues' reliance on a continuous oxygen supply for its function considering that the high metabolic rate and oxidative metabolism is the tissue's major source of energy and their lack of oxygen stores (Terraneo and Samaj, 2017).…”

Section: Hypoxia Actions On Brain Tissuementioning

confidence: 99%

Hypoxia-Induced Cardiac Arrest Alters Central Nervous System Concentrations of the GLYT2 Glycine Transporter in Zebrafish (Danio rerio)

Auzenne

View full text Add to dashboard Cite

Hypoxia as a stressor has physiological implications that have been a focal point for many physiological studies in recent years. In some studies, hypoxia had large effects on the organ tissue degeneration, which ultimately effects multiple ecological processes. These organ tissue studies played a part in the development of new fields like neurocardiology, a specialty that studied the relationship between the brain and the heart. This thesis focuses on how hypoxia-induced cardiac arrest alters the amounts of GLYT2, a glycine reuptake transporter, in the central nervous system of zebrafish, Danio rerio. At 7 days post-fertilization (dpf), zebrafish were exposed to acute, severe hypoxia until they lost equilibrium, and minutes later, subsequent cardiac arrest occurred. Zebrafish were then placed into recovery groups to measure the GLYT2 levels at multiple points in zebrafish recovery. Fish were then sacrificed, and their brains dissected. Using immunofluorescence, the outer left optic tectum of the zebrafish was imaged, and mean image pixel fluorescent intensity was taken. There were significant changes (one-way ANOVA) in the levels of GLYT2 compared to that of the control groups during the course of recovery. GLYT2 levels continued to rise through the 24-hour recovery mark but did not show significant difference after 3 hours of recovery. This suggest that GLYT2 levels increased rapidly in the first 3 hours of recovery and continued to increase through 24 hours at a slower rate. Changes in GLYT2 levels may affect motor and sensory information, movement, visualization, and audition in these zebrafish. Further research should be conducted to determine how long it takes for GLYT2 levels to return to baseline, as well as behavioral measurements through each recovery period as it relates to glycine function.

show abstract

Hypercapnic hypoxia improves cognitive and motor functions of children with cerebral palsy

Cited by 4 publications

References 27 publications

Neuroprotective effect of hypoxic-hypercapnic training. Review

Neuroprotective effect of hypoxic-hypercapnic training. Review

Molecular Mechanisms of Neuroprotection after the Intermittent Exposures of Hypercapnic Hypoxia

Hypoxia-Induced Cardiac Arrest Alters Central Nervous System Concentrations of the GLYT2 Glycine Transporter in Zebrafish (Danio rerio)

Contact Info

Product

Resources

About