hyperoxia/seizures

Hyperoxia beyond 1.8 ATA results in a striking reduction of high-pressure neurological syndrome (HPNS) type I convulsion threshold pressures but is without measurable effect on type II convulsions. The synergism is partially or completely reversed by increasing alveolar or tissue CO2 levels. High

Hyperoxia brought about substantial accumulation of primary and end products of lipid peroxidation (LPO) and a significant lowering of alpha-tocopherol content in rat brain tissues. Preinjection of animals with synthetic and natural antioxidants (4-methyl-2,6-ditretbutylphenol and alpha-tocopherol)

Oxygen is the most widely used therapeutic strategy to prevent and treat decompression sickness (DCS). Oxygen prebreathe (OPB) eliminated DCS in 20-kg swine after rapid decompression from saturation at 60 feet of seawater (fsw). However, hyperbaric oxygen (HBO) has risks. As oxygen partial pressure

The endogenous vasodilator and signaling molecule nitric oxide has been implicated in cerebral hyperemia, sympathoexcitation, and seizures induced by hyperbaric oxygen (HBO2) at or above 3 atmospheres absolute (ATA). It is unknown whether these events in the onset of central nervous system oxygen

BACKGROUND Preoxygenation and hyperventilation (with oxygen) in electroconvulsive therapy (ECT) may improve not only safety but also seizure quality. METHODS We retrospectively examined transcutaneous tissue partial pressure of oxygen (tcpO2) and carbon dioxide (tcpCO2) in 441 ECT sessions of 37

Hyperbaric oxygen (HBO(2)) stimulates presumptive central CO2-chemoreceptor neurons, increases minute ventilation (V(min)), decreases heart rate (HR) and, if breathed sufficiently long, produces central nervous system oxygen toxicity (CNS-OT; i.e., seizures). The risk of seizures when breathing

Two hundred suckling mice from 20 litters were used for determining their functional development of the hyperoxic convulsion mechanism. It was found that 1 to 12-day-old mice did not develop convulsion when they were subjected to oxygen under high pressure. The hyperoxic convulsion was observed in 1

Age is a natural factor that has been found to significantly affect sensitivity to hyperbaric hyperoxia (HBO). Exposure to HBO may lead to damages in the energy metabolism of the brain cells. The aim of this study was to test the effect of HBO on the metabolic, hemodynamic and electrical activities

The total Mg2+-ATPase and Na+, K+-ATPase activity was studied in the fractions of "400 g X for 20 min" and "900 g X for 30 min" conditionally called the fraction of the external cellular membranes and total fraction of mitochondria. The subcellular fractions were isolated from great hemispheres and

Experiments in 104 white mice subjected to hyperoxia at different regimens of oxygenation, carried out by means of mathematical modelling of three hyperoxic effects (bradypnea, convulsions, lethality) revealed the dependence of biological (physiological, toxic) effects of hyperoxia upon both

BACKGROUND It was hypothesized that long-duration exposures to toxic levels of hyperoxia would have effects on respiratory control function or activity. METHODS Ventilatory parameters of human subjects breathing spontaneously at rest were measured before, during, and after hyperoxia in a study of

Double-beam recording visible cytospectrophotometry showed that 30-minute convulsions due to 6 at. ga. hyperoxia result in a decrease in the RNA and protein content per cell in layer V neurons of the cerebral motor cortex and in the motoneurons of spinal cord anterior horn in albino rats. A decrease