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George Mychaskiw

Publications and source records attributed to George Mychaskiw.

11 recordsLinked to original sources
PubMed2005

Mechanisms of hyperbaric oxygen and neuroprotection in stroke.

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 3-6h 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.

Journal Article↗
PubMed2005

Effects of hyperbaric oxygen on skin blood flow and tissue morphology following sciatic nerve constriction.

BACKGROUND: Constriction of the sciatic nerve by loose ligation produces an inflammatory neuropathic injury. This represents an animal model for peripheral mononeuropathy. Oxygen-derived free radicals are suspected to play an important role in the pathogenesis of ischemia/reperfusion injury, leading to neurogenic inflammation. Hyperbaric oxygen (HBO) has been used anecdotally to treat clinically similar conditions in humans, but specific effects on the animal model have not been well studied. OBJECTIVE: This study in a rat model examined the effects of hyperbaric oxygen on skin blood flow and tissue morphology by light and electron microscopy following sciatic nerve constriction. DESIGN: A scientific investigation in a rat model. METHODS: In this study, the neuropathic injury was established by loose ligation of the rat sciatic nerve. The animals were divided into three groups, sham (S, n=8), ligation but no treatment (LN, n=8) and ligation and treatment with hyperbaric oxygen (LT, n=8). The treatment group (n=8) received hyperbaric oxygen treatment immediately following the injury and daily for four additional days at the same time interval. One hundred percent O2 at 3 atmospheres absolute pressure (66 feet sea water) was administered for two hours. The hindpaws of the rats were observed by light microscopy, electron microscopy, laser Doppler flowmetry (LDF), and clinically for the presence of edema. RESULTS: Untreated animals demonstrated marked tissue edema following sciatic constriction, whereas animals that received hyperbaric oxygen had minimal to no edema. The sham group demonstrated normal histology. The group not treated with hyperbaric oxygen demonstrated swollen mitochondria (2-3 times), with loss of cellular integrity, multiple vacuole formation in both nerve and muscle tissue, widened sarcomeres in muscle, and degenerative changes in the nerve myelin sheaths. The group treated with hyperbaric oxygen demonstrated preservation of cellular structure including mitochondrial integrity, no vacuole formation, and maintenance of normal, easily identifiable nerve structure. The sham group had no change of skin blood flow. Skin blood flow of LT group was decreased immediately after ligation (p<0.05) and recovered to baseline level before ligation on Day 5 after four hyperbaric oxygen treatments. Skin blood flow of LN group was decreased immediately after ligation (p <0.01) and did not recover (p <0.01). CONCLUSION: This study evaluated tissue changes after nerve injury caused by loose ligation of the sciatic nerve in rats. Hyperbaric oxygen treatment following sciatic nerve injury reduced tissue edema, improved skin blood flow, and preserved muscle and neuronal ultrastructural integrity.

Journal Article↗
PubMed2002

Hyperbaric oxygenation prevented brain injury induced by hypoxia-ischemia in a neonatal rat model.

The occurrence of hypoxia-ischemia (HI) during early fetal or neonatal stages of an individual leads to the damaging of immature neurons resulting in behavioral and psychological dysfunctions, such as motor or learning disabilities, cerebral palsy, epilepsy or even death. No effective treatment is currently available and this study is the first to use hyperbaric oxygen (HBO) as a treatment for neonatal HI. Herein, we sought out to determine if HBO is able to offer neuroprotectivity against an HI insult. Seven-day-old rat pups were subjected to unilateral carotid artery ligation followed by 2.5 h of hypoxia (8% O(2) at 37 degrees C). HBO treatment was administered by placing pups in a chamber (3 ATA for 1 h) 1 h after hypoxia exposure. Brain injury was assessed based on ipsilateral hemispheric weight divided by contralateral hemispheric weight, light microscopy, and EM. Sensorimotor functional tests were administered at 5 weeks after hypoxia exposure. After HI, the ipsilateral hemisphere was 52.65 and 57.64% (P<0.001) of the contralateral hemisphere at 2 and 6 weeks, respectively. In HBO treated groups, the ipsilateral hemisphere was 77.77 and 84.19% (P<0.001) at 2 and 6 weeks. There was much less atrophy and apoptosis in HBO treated animals under light or electron microscopy. Sensorimotor function was also improved by HBO at 5 weeks after hypoxia exposure (Chi-square, P<0.050). The results suggest that HBO is able to attenuate the effects of HI on the neonatal brain by reducing the progression of neuronal injury and increasing sensorimotor function.

Animals↗
PubMed2002

Down regulation of COX-2 is involved in hyperbaric oxygen treatment in a rat transient focal cerebral ischemia model.

The effect of hyperbaric oxygen (HBO) on cyclooxygenase-2 (COX-2) expression after transient focal ischemia was evaluated. A rat middle cerebral artery occlusion/reperfusion (MCAO) model was produced using the intraluminal filament method. After 2 h of occlusion, 24 h of reperfusion, brains were removed. Three atmospheres absolute HBO for 1 h was administered at 6 h after reperfusion. The infarct volume was evaluated by 2,3,7-triphenyltetrazolium chloride staining. COX-2 mRNA expression was measured by reverse transcription polymerase chain reaction, and COX-2 protein expression was analyzed by Western blot. The results showed that HBO applied at 6 h after reperfusion significantly reduces infarct area as compared with no-treatment group. HBO decreased COX-2 mRNA and protein levels, which were upregulated after ischemia/reperfusion. HBO had no direct effect on COX-2 protein expression in matched normal rats. We conclude that (1) early intervention with HBO within 6 h reduces infarction. (2) The neuroprotective effect of HBO might lead to an inhibition of COX-2 over-expression in cerebral cortex.

Animals↗