Introduction
Oxygen
Mechanism underlying the theraputic effects of hyperoxia
Hyperoxia increases oxygen supply
Hyperoxia on the hemodynamics
Hyperoxia on energy metabolism
Hyperoxia on the inflammatory process
Hyperoxia on delayed cell death
Hyperoxia on vascular permeability
Hyperoxia on the plasticity process
Neuroclinical application of oxygen therapy
Normobaric hyperoxia on traumatic brain injury
Normobaric hyperoxia on stroke
Hyperbaric oxygen on traumatic brain injury
Hyperbaric oxygen on ischemic stroke
Hyperoxia Pre-Conditioning
Mechanisms underlying the protective effects of hyperoxia pre-conditioning
Application of hyperoxia pre-conditioning
Oxygen toxicity
Helium
Introduction
Biological effects of helium and potential mechanisms
BIOLOGICAL EFFECTS | POTENTIAL MECHANISMS |
---|---|
Coronary Collateral Circulation | Prosurvival Signaling Kinases [137] |
Improve Exercise Tolerance
| MPTP Opening [139] |
Anti-Arrhythmic Effect
| Mitochondrial Uncoupling [136] |
Anti-Tumor Effect
| |
Anti-Inflammation
| |
Hypothermia
| |
High Pressure Nervous Syndrome
| Mitochondrial Permeability Transition [139] |
Neuroprotective Effect
| Opioid Receptors [140] |
Myocardioprotective Effect
| COX-2 Activity [23] |
Application of helium in neurology
Xenon
Biological effects of xenon and potential mechanisms
Application of xenon in neurology
Model | Intervention | Results | Reference |
---|---|---|---|
NMDA, glutamate, or oxygen deprivation induced neuronal injury | Xenon saturated medium for 24 h (in vitro) 20%, 40%, 60%, 75% xenon (in vivo) | Xenon (60% atm) reduces LDH release to baseline with oxygen deprivation; xenon (75% atm) reduces LDH release by 80% with either NMDA-or glutamate-induced injury. In vivo, xenon exerts a concentration-dependent protective effect and reduces injury by 45% at the highest xenon concentration tested (75% atm). | [170] |
Hypoxia damaged cortical neurons from rat embryos | Xenon saturated medium for 2 h | Complete protection against cellular damage and prevention of hypoxia-induced glutamate release | [171] |
Hypoxia damaged PC-12 cells | Xenon saturated medium for up to120 min | Xenon results in complete protection against cellular damage and prevention of hypoxia-induced dopamine release in which intracellular Ca2+-ions evolve. | [172] |
MCAO in mice | 70%, 35% xenon during occlusion for 60 min | Xenon administration improves both functional and histological outcome | [173] |
Neonatal HI | 70%, 50% xenon immediately after insult for 3 h | Xenon administration commenced after hypoxia-ischemia in neonatal rats provides short-term neuroprotection | [174] |
brain slices from rats (OGD) MCAO | 15-75% xenon bubbled medium 50% xenon 2~3 h after MCAO | Xenon, administered at subanesthetic doses, offers global neuroprotection from reduction of neurotransmitter release induced by ischemia, reduces subsequent cell injury and neuronal death | [175] |
NMA induced neuronal damage | 70% xenon for 10 min at 3 h, 1, 2, 5, or 7 days before insult | Xenon alone does not induce changes, but reduces about 50% NMDA-induced cell loss as well as degenerating neurons, with the maximal neuroprotection at 7 days. | [176] |
anesthetic-induced neuronal apoptosis in vivo and in vitro | 75%, 60%, 30% xenon for 6 h | Xenon attenuates isoflurane-induced apoptosis. | [164] |
nitrous oxide and isoflurane induced damage | 70% xenon for 2 h | Xenon pre-treatment prevents nitrous oxide-and isoflurane-induced neuroapoptosis (in vivo and in vitro) and cognitive deterioration (in vivo) | [165] |
OGD induced damage to neurons from neonatal mice | 75% xenon + Dex (0.001~10 μM) for 6 h | Combination of Xenon and Dex offers neuroprotection additively in vitro and synergistically in vivo | [178] |
neonatal HI | 20-70% xenon for 90 min during hypoxia or 2, 24 h after hypoxia + hypothermia (30-37°C) | Xenon and hypothermia administered 4 h after hypoxic-ischemic injury in neonatal rats provides synergistic neuroprotection | [177] |
OGD induced damage to neurons; neonatal HI | 25~75% xenon for 120 min (in vitro); 70% xenon for 120 min (in vivo) | Prosurvival proteins Bcl-2 and brain-derived neurotrophic factor are upregulated by xenon treatment | [179] |
OGD induced damage to neurons; neonatal HI | 12.5~75% xenon for 2 h (in vitro); 20%, 75% for 2 h (in vivo) | Pre-conditioning with xenon and the combination of xenon and sevoflurane results in long-term functional neuroprotection associated with enhanced phosphorylated cyclic adenosine monophosphate response element binding protein signaling | [180] |
MCAO in mice | 70% xenon for 2 h | Xenon pre-conditioning improves histological and neurological functional outcome in both genders in a stroke model of mice in which HIF-1α and phosphoAkt evolve | [207] |
OGD induced damage to neurons | 75% xenon for 2 h | Xenon pre-conditioning clearly involves the activation of KATP channels. | [208] |
Hydrogen
Mechanisms underlying the bioeffects of hydrogen
Application of hydrogen in neurology
Model | Intervention | Results | Reference |
---|---|---|---|
MCAO | 1%, 2%, 4% hydrogen during the occlusion (85 min), or reperfusion (35 min) or occlusion + reperfusion (120 min) | Inhalation of hydrogen markedly suppresses brain injury by buffering the effects of oxidative stress. 2% hydrogen is more effective than 4% and 1% hydrogen | [190] |
neonatal HI | 2% hydrogen (30, 60 and 120 min) or hydrogen saturated saline (5 ml/kg immediately and 8 h after insult) | Hydrogen treatment significantly reduces the apoptotic cells, suppresses caspase-3 and -12 activities, reduces MDA and Iba-1 levels, and improves the long-term neurological and neurobehavioral functions | |
newborn pig asphyxia | 2.1% H2-supplemented room air for 1 h and additional 3 h | H2-RA ventilation significantly increases cerebrovascular reactivity to hypercapnia after asphyxia/reventilation; no affects on ROS-dependent cerebrovascular reactivity to NMDA | [209] |
neonatal HI MCAO | Inhalation of 2.9% hydrogen | Inhalation of 2.9% hydrogen did not decrease the infarction volume and brain lipid peroxidation, but there was a trend suggesting a beneficial effect on MCAO in adult rats | [196] |
hypoxia-reoxygenation of brain slices of vitamin C-depleted SMP30/GNL knockout mice | hydrogen-rich pure water | Hydrogen-rich pure water acts as an anti-oxidant and prevents superoxide formation | [197] |
amyloid-β-induced Alzheimer's disease | Intraperitoneal hydrogen rich saline (5 ml/kg daily for 2 weeks) | Hydrogen-rich saline prevents beta-induced neuroinflammation and oxidative stress, which may contribute to the improvement of memory dysfunction in this rat model | [198] |
MCAO | Inhalation of 2.9% hydrogen during reperfusion | Inhalation of hydrogen during 2 h reperfusion was found to reduce brain infarction, hemorrhagic transformation, and improve neurological function | [199] |
chronic physical restraint in mice | Oral intake of hydrogen supplemented water up to 8 weeks | Hydrogen water reduces oxidative stress in the brain, and prevents the stress-induced decline in learning and memory caused by chronic physical restraint | [200] |
MPTP induced Parkinson's disease model | Oral intake of hydrogen containing water for 28 days | Drinking hydrogen-containing water significantly reduces the loss of dopaminergic neurons accompanied by significant reduction of oxidative stress which was demonstrated by a significant decrease of DNA damage and lipid peroxidation. | [201] |
6-OHDA induced Parkinson's disease model | Oral intake of hydrogen containing water before and after surgery | Prevent both the development and progression of the nigrostrital degeneration and dopaminergic cell loss | [202] |
Senescence-accelerated mice | Oral intake of hydrogen containing water for 30 days and 18 weeks | Prevented age-related declines in cognitive ability increases brain serotonin levels and elevates serum antioxidant activity at 30 days while inhibiting neurodegeneration in the hippocampus at 18 weeks | [203] |