ALSUntangled No. 35: Hyperbaric Oxygen Therapy* (original) (raw)
Related papers
Reflections on the neurotherapeutic effects of hyperbaric oxygen
Expert Review of Neurotherapeutics, 2014
Traumatic brain injury (TBI) and stroke are the major causes of brain damage and chronic neurological impairments. There is no agreed-upon effective metabolic intervention for TBI and stroke patients with chronic neurological dysfunction. Clinical studies published this year present convincing evidence that hyperbaric oxygen therapy (HBOT) might be the coveted neurotherapeutic method for brain repair. Here we discuss the multi-faceted role of HBOT in neurotherapeutics, in light of recent persuasive evidence for HBOT efficacy in brain repair and the new understanding of brain energy management and response to damage. We discuss optimal timing of treatment, dosage, suitable candidates and promising future directions.
An Extra Breath of Fresh Air: Hyperbaric Oxygenation as a Stroke Therapeutic
Biomolecules, 2020
Stroke serves as a life-threatening disease and continues to face many challenges in the development of safe and effective therapeutic options. The use of hyperbaric oxygen therapy (HBOT) demonstrates pre-clinical effectiveness for the treatment of acute ischemic stroke and reports reductions in oxidative stress, inflammation, and neural apoptosis. These pathophysiological benefits contribute to improved functional recovery. Current pre-clinical and clinical studies are testing the applications of HBOT for stroke neuroprotection, including its use as a preconditioning regimen. Mild oxidative stress may be able to prime the brain to tolerate full extensive oxidative stress that occurs during a stroke, and HBOT preconditioning has displayed efficacy in establishing such ischemic tolerance. In this review, evidence on the use of HBOT following an ischemic stroke is examined, and the potential for HBOT preconditioning as a neuroprotective strategy. Additionally, HBOT as a stem cell prec...
Journal of the Formosan Medical Association, 2014
Background/Purpose: Repetitive hyperbaric oxygen (HBO 2) therapy may cause excessive generation of reactive oxygen species. This study assessed whether repetitive or 2e4-day trials of HBO 2 therapy (2 treatments daily for 2e4 consecutive days) provides better effects in reducing brain inflammation and oxidative stress caused by middle cerebral artery occlusion (MCAO) in rats than did a 1-day trial of HBO 2 therapy (2 treatments for 1 day). Methods: Rats were randomly divided into four groups: sham; MCAO without HBO 2 treatment; MCAO treated with 1-day trial of HBO 2 ; and MCAO treated with 2e4-day trials of HBO 2. One treatment of HBO 2 (100% O 2 at 253 kPa) lasted for 1 hour in a hyperbaric chamber. Results: Therapy with the 2e4-day trials of HBO 2 significantly and dose-dependently attenuated the MCAO-induced cerebral infarction and neurological deficits more than the 1-day trial of HBO 2 therapy. The beneficial effects of repetitive HBO 2 therapy were associated with: (1) reduced inflammatory status in ischemic brain tissues (evidenced by decreased levels of tumor necrosis factor-a, interleukin-1b, and myeloperoxidase activity); (2) decreased oxidative damage in ischemic brain tissues (evidenced by decreased levels of reactive oxygen and nitrogen species, lipid peroxidation, and enzymatic pro-oxidants, but increased levels of enzymatic antioxidant defenses); and (3) increased production of an anti-inflammatory cytokine, interleukin-10.
2010
The present study examined the eVect of hyperbaric oxygen (HBO) on the formation of 2,3-dihydroxybenzoic acid (2,3-DHBA) and 2,5-dihydroxybenzoic acid (2,5-DHBA), the products of salicylate trapping of hydroxyl free radicals, and glutamate release in the striatum during acute ischemia and reperfusion. Non-HBO rats (n = 8) were subjected to 1-h ischemia. Study rats (n = 8) were treated with HBO at 2.8 ATA for 1 h during ischemia. ArtiWcial CSF solution containing 5 mM sodium salicylate was perfused at 1 l/min. Samples were continuously collected at 15 min intervals and the levels of 2,3-DHBA, 2,5-DHBA, and glutamate were analyzed. The lesion volume was determined by TTC stain. Occlusion of the middle cerebral artery induced a signiWcant increase in the levels of 2,3-DHBA and 2,5-DHBA. A peak of approximately two and fourfold of baseline levels was reached at 45 min and was maintained at elevated levels during reperfusion. The level of glutamate increased approximately two times at 30 min during ischemia, continued to increase, and reached approximately three times baseline level during reperfusion. HBO signiWcantly alleviated brain injury associated with decreased levels of 2,3-DHBA, 2,5-DHBA and glutamate. This study suggests that the decreased glutamate release and the reduced formation of hydroxyl free radicals might contribute to the neuroprotective eVect of HBO.
Hyperbaric Oxygen Therapy: Exploring the Clinical Evidence C L I N I C A L M A N A G E M E N T extra
All tests are now online only; take the test at http://cme.lww.com for physicians and www.nursingcenter.com for nurses. Complete CE/CME information is on the last page of this article. GENERAL PURPOSE: To provide information about hyperbaric oxygen therapy (HBOT), its mechanisms, indications and safe applications based on clinical evidence. TARGET AUDIENCE: This continuing education activity is intended for physicians, physician assistants, nurse practitioners, and nurses with an interest in skin and wound care. LEARNING OBJECTIVES/OUTCOMES: After participating in this educational activity, the participant should be better able to: 1. Recall the physiology of wound healing and the mechanisms of action of HBOT. 2. Identify current applications of HBOT based on clinical evidence as well as its risks and contraindications. ABSTRACT Treating chronic wounds and infections are challenging medical problems worldwide. Hyperbaric oxygen therapy (HBOT), the administration of 100% oxygen at pressures greater than 1.4 atmosphere absolute in a series of treatments, can be used as an adjunctive therapy in many wound care settings because it improves oxygenation and neovascularization and decreases inflammation in chronic wounds. A growing number of studies support the benefits of HBOT for enhancing wound healing and decreasing the likelihood of negative events such as amputation. However, many practitioners are unfamiliar with HBOT. This article provides a general introduction to HBOT, reviews the physiology and mechanisms of behind HBOT, discusses all the indications for HBOT, and explores in-depth the clinical evidence for HBOT in the treatment of arterial insufficiencies, diabetic ulcers, delayed radiation injury, and chronic refractory osteomyelitis.
The effect of hyperbaric oxygen therapy on the nervous system. Systematic review
Polish Hyperbaric Research, 2015
Hyperbaric oxygen therapy (HBOT) is found among the interests of researchers who seek new methods of treatment of diseases of the nervous system. An increase of the partial pressure of oxygen in arterial blood within the appropriate range leads to numerous changes in the cells of the brain tissue. In this paper we analyse the results of selected articles describing HBOT used on pathologies of the nervous system such as stroke, autism, multiple sclerosis and cerebral palsy as well as in the course of research on animal models. The results are promising, although some studies struggled with numerous methodological problems and differences in the applied protocols, which resulted in conflicting results in individual interventions. In consequence, the need for further studies in randomised control trials and determination of the protocol by an international group of researchers dedicated to the use of HBOT was emphasised.
Neuroscience, 2003
The Wobbler mouse is a model of human motor neuron disease. Recently we reported the impairment of mitochondrial complex IV in Wobbler mouse CNS, including motor cortex and spinal cord. The present study was designed to test the effect of hyperbaric oxygen therapy (HBOT) on (1) mitochondrial functions in young Wobbler mice, and (2) the onset and progression of the disease with aging. HBOT was carried out at 2 atmospheres absolute (2 ATA) oxygen for 1 h/day for 30 days. Control groups consisted of both untreated Wobbler mice and non-diseased Wobbler mice. The rate of respiration for complex IV in mitochondria isolated from motor cortex was improved by 40% (P<0.05) after HBOT. The onset and progression of the disease in the Wobbler mice was studied using litters of pups from proven heterozygous breeding pairs, which were treated from birth with 2 ATA HBOT for 1 h/day 6 days a week for the animals' lifetime. A "blinded" observer examined the onset and progression of the Wobbler phenotype, including walking capabilities ranging from normal walking to jaw walking (unable to use forepaws), and the paw condition (from normal to curled wrists and forelimb fixed to the chest). These data indicate that the onset of disease in untreated Wobbler mice averaged 36؎4.3 days in terms of walking and 40؎5.7 days in terms of paw condition. HBOT significantly delayed (P<0.001 for both paw condition and walking) the onset of disease to 59؎8.2 days (in terms of walking) and 63؎7.6 days (in terms of paw condition). Our data suggest that HBOT significantly ameliorates mitochondrial dysfunction in the motor cortex and spinal cord and greatly delays the onset of the disease in an animal model of motor neuron disease.
Mechanisms of hyperbaric oxygen and neuroprotection in stroke
Pathophysiology, 2005
Cerebral vascular diseases, such as neonatal encephalopathy and focal or global cerebral ischemia, all result in reduction of blood flow to the affected regions, and cause hypoxia-ischemia, disorder of energy metabolism, activation of pathogenic cascades, and eventual cell death. Due to a narrow therapeutic window for neuroprotection, few effective therapies are available, and prognosis for patients with these neurological injuries remains poor. Hyperbaric oxygen (HBO) has been used as a primary or adjunctive therapy over the last 50 years with controversial results, both in experimental and clinical studies. In addition, the mechanisms of HBO on neuroprotection remain elusive. Early applications of HBO within a therapeutic window of 3-6 h or delayed but repeated administration of HBO can either salvage injured neuronal tissues or promote neurobehavioral functional recovery. This review explores the discrepancies between experimental and clinical observations of HBO, focusing on its therapeutic window in brain injuries, and discusses the potential mechanisms of HBO neuroprotection.