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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inert gas narcotics increase intrinsic pressure tolerance (1,000Pc) in CD-1 mice but interfere with development of the protective responses raising seizure thresholds during slower compression (e.g., 60Pc). This secondary narcotic effect can block up to 40% of the total attainable increase in Pc. The narcosis susceptible moiety of this compression rate effect develops early, whereas a narcosis resistant remnant accounts for increase in Pc occurring after 90 min of compression or pressure exposure. Pressure conditioning by multiday pressure exposure entails increases in both 60Pc and 1,000Pc and in virtual annullment of the compression rate effect. The effect can be completely blocked by narcotic gases in the conditioning atmosphere. In addition to blocking part of the compression rate effect the presence of narcotic gases under these conditions can reverse the effects of previously established pressure conditioning. 60Pc regresses much more slowly under these conditions than 1,000Pc. Either reversal rate is much more rapid in air at 1 ATA than at 80 ATA under 0.9 atm N2O. The implications of these data are discussed with regard to evaluation of the hypothesis of antagonism between inert gas narcotics and high pressures and to elaboration of the monoamine hypothesis to account for the modification of the compression rate effect by narcotic gases.
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PMID:Opposing effects of anesthetics on pressure tolerance and compression rate effect. 359 35

Central nervous system oxygen toxicity in hyperbaric oxygen-inert gas mixtures was studied by exposing male rats to various gas mixtures having the same oxygen partial pressure and varying pressures of inert gases. The duration of the latent period until the appearance of electrical discharges in the electroencephalogram was used as the criterion for the sensitivity to CNS oxygen toxicity. Two hundred and twenty rats with chronically implanted cortical electrodes were subjected to a single exposure to 1 of 11 different gas mixtures at ambient pressures ranging from 5 to 10 ATA. All gas mixtures had a constant oxygen partial pressure of 5 ATA and varying pressures of inert gas (helium or nitrogen). The duration of the latent period was found to be significantly different in the 11 experimental groups (P less than 0.001). While increasing the inert gas pressure, the latency gradually shortened, reaching the lowest values in mixtures of 5 ATA oxygen and 3 ATA of either inert gas. On further increase in the inert gas pressure up to a total ambient pressure of 10 ATA, the latency returned to control (pure 5 ATA oxygen) values. No difference was found between nitrogen and helium of equal partial pressures. These findings suggest that the risk of CNS oxygen toxicity in gas mixtures is not determined solely by the PO2, and even a relatively low pressure of inert gas can contribute to the imminence of hyperbaric-oxygen-induced seizures.
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PMID:CNS oxygen toxicity in oxygen-inert gas mixtures. 368 42

Multiday exposures of CD-1 mice to He-O2 atmospheres at pressures from 30 to 100 atm result in marked increases of threshold pressures for type I high-pressure neurological syndrome seizures. The effect develops with a half time (t1/2) of 12 h and is reversible (t1/2 = 7 h). The maximum enhancement of Pc is attained at a conditioning pressure of 80 ATA. Pressure conditioning also results in suppression of the compression rate effect on Pc. Furthermore, reserpine blocks the increase in Pc during prolonged pressure exposure. The entire effect thus appears to be an extension in time of the monoaminergic compression rate effect on Pc. Pressure conditioning does not modify anesthesia tolerance, unlike N2 habituation which affects anesthesia threshold pressure as well as Pc. The results are compared with the effects of habituation to inert-gas narcotics and the implications of the data for an understanding of inert-gas high-pressure antagonism in intact animals are discussed.
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PMID:Prolonged exposure of mice to He-O2 at high pressure: effects on seizure and anesthesia liability. 380 8

High hydrostatic pressure has been shown to produce neurological changes in humans which manifest, in part, as tremor, myoclonic jerks, electroencephalographic changes, and convulsions. This clinical pattern has been termed high-pressure nervous syndrome (HPNS). These symptoms may represent an alteration in synaptic transmission in the central nervous system with the inhibitory neural pathways being affected in particular. Since gamma-aminobutyric acid (GABA) transmission has been implicated in other seizure disorders, it was of interest to study GABAergic function at high pressure. Isolated synaptosomes were used to follow GABA release at 67.7 ATA of pressure. The major observation was a 33% depression in total [3H]GABA efflux from depolarized cerebrocortical synaptosomes at 67.7 ATA. The Ca2+-dependent component of release was found to be completely blocked during the 1st min of [3H]GABA efflux with a slow rise over the subsequent 3 min. These findings lead us to conclude that high pressure interferes with the intraterminal cascade for Ca2+-dependent release of GABA.
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PMID:Effect of pressure on [3H]GABA release by synaptosomes isolated from cerebral cortex. 380 14

The kindling effect is an experimental model of epilepsy which results from an intermittent application of focal electrical stimulations to certain regions of the brain. Generalized seizures are usually obtained after about fifteen stimulations of amygdala in the rat. We studied the kindling effect in hyperbaric-hyperoxic conditions. Eleven Wistar rats were stimulated daily in a caisson and all stimulations were delivered after 30 min of diving at 3 ATA of air. Diving inhibited kindling in half animals. In the others, which all presented generalised convulsions, diving produced a reduction in seizure duration, especially during the generalisation phase.
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PMID:[Epileptogenesis caused by the kindling effect in diving at 3 ATA of air]. 402 Jul 11

Exposure to oxygen at pressures greater than 2.8 ATA (OHP) results in central nervous system toxicity seen as grand mal seizures. The time to onset of seizures (ts) is related to the pO2 above the 2.8 ATA threshold. The components of the endogenous antioxidant defense mechanism, superoxide dismutase (SOD), glutathione measured here as nonprotein sulfhydryl content (NPSH), glucose-6-phosphate dehydrogenase (G-6-PD), glutathione reductase (GR), and glutathione peroxidase (GPx) occur in brain. Their role in OHP-induced CNS toxicity is not clear. This study examined the effect of inhibition of SOD by diethyldithiocarbamate (DDC) on ts at 4 ATA O2. Antioxidant components (SOD, NPSH, G-6-PD, GR, and GPx) were measured in male Sprague-Dawley rats pretreated with 250, 500, and 1000 mg/kg DDC ip, 2 hr prior to termination in room air. SOD activity was inhibited 11, 31, and 49%, respectively, when compared with control values. Among the other antioxidant components, only GPx showed a significant loss of activity of 24% at 1000 mg/kg DDC. Rats were also pretreated 2 hr prior to exposure to hyperbaric oxygen with either 250, 500, or 1000 mg/kg DDC. Ts for the treated animals was significantly shortened by 12, 55, and 75%, respectively, compared to the saline-treated, oxygen-exposed control animals. These studies demonstrated that the rate of onset of CNS oxygen toxicity was increased by inhibition of SOD by DDC. These data suggested that SOD plays a role as part of an endogenous antioxidant defense mechanism in the brain.
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PMID:Influence of rat brain superoxide dismutase inhibition by diethyldithiocarbamate upon the rate of development of central nervous system oxygen toxicity. 608 74

Cells that utilize molecular oxygen generate highly reactive oxygen-derived free radicals. Endogenous cellular oxidants inactivate oxidant free radicals and protect aerobic cells from oxidant injury. Glutathione, glutathione reductase, and superoxide dismutase are key components of this antioxidant defense. Inhibition of antioxidant components would be expected to result in cell injury. Using exposure to oxygen at high pressure to increase the level of oxidant free radicals, evidence is presented to support the hypothesis that inhibition of cellular antioxidants renders organisms more susceptible to oxygen toxicity. Diethyldithiocarbamate at doses of 250, 500 and 1000 mg/kg inhibited rat brain superoxide dismutase activity and shortened onset time to seizures in a dose-related manner in 4 ATA oxygen. Carmustine at doses of 12.5, 25 and 50 mg/kg inhibits glutathione reductase activity in rat brain in proportion to the dose. Time to onset of seizures of rats pretreated with carmustine prior to exposure to 4 ATA oxygen was shortened, and oxidized glutathione levels were increased in the cortex and subcortex. These data suggest that inhibition of antioxidant components results in organisms becoming more sensitive to oxygen toxicity. Compounds that inhibit cellular antioxidants may produce toxic cell injury by permitting intracellular oxidant free radicals to attack essential cell constituents.
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PMID:Inhibition of cellular antioxidants: a possible mechanism of toxic cell injury. 609 75

Previous studies have shown that sympathetic factors and blood glucose are of importance in the development of seizures and lung damage from OHP. In the present study we examined the influence of beta sympathetic agonists and blocking agents and glucagon on OHP toxicity. Rats were exposed to 6 ATA OHP and examined for time-to-seizure and lung damage. Pretreatment with propranolol increased the time-to-seizure by 70% and practolol by 50% without altering gross lung appearance or lung wet wt/dry wt. Propranolol and practolol also prevented brain glycogen depletion prior to seizure which otherwise occurred in subconvulsive exposure to OHP. Isoproterenol and glucagon pretreatment had no effect on time-to-seizure but isoproterenol did increase lung injury. Both practolol and propranolol block the beta-receptor influence on adenyl cyclase-stimulated second messenger production, while both isoproterenol and glucagon activate adenyl cyclase to produce second messenger. Our results may suggest a possible role for second messenger in mediating some of the acute toxic effects of OHP on the CNS.
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PMID:Beta adrenergic receptors and glucagon in seizures from exposure to oxygen at high pressure (OHP). 631 53

General anesthetics, ganglionic blocking agents, anticonvulsants, and antioxidants have been shown to afford protection from seizures caused by exposure to hyperbaric oxygen. In the present study cats were exposed to 5 ATA oxygen in pairs in a hyperbaric chamber until both the control and pretreated cat convulsed or for a maximum 120 min exposure. Small amounts of four common antiepileptic agents and propylene glycol in amounts far less than previously reported (0.1 to 0.2 ml/kg) were initially tested for potential anticonvulsant activity. Two agents, clonazepam and propylene glycol, offered significant protection in delaying the onset of seizures whereas carbamazepine, valproic acid, and trimethadione appeared to hasten the onset of seizure activity. The time to seizures was increased nearly five times by clonazepam and over three times by very small amounts of propylene glycol.
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PMID:Protection from oxygen-induced seizures by clonazepam and propylene glycol. 679 72

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 total pressures (PI) result in striking reductions in the duration of hyperoxic exposure preceding seizure onset (tc). The interaction of hyperoxia and high pressure gives rise to three zones on the PO2-Pt plane. In zone I, Pt less than 30 ATA, the duration of hyperoxia prior to convulsion onset is given by the equation PO2 -- PO2 lim = K/(tc -- tc lim), where PO2 lim and tc lim both decrease with increasing total pressure. Zone II, Pt = 30-50 ATA and PO2 1.8-2.3 ATA, is characterized by a sharp drop in tc, as Pt is increased beyond 30 ATA, to a value near 15 min that is constant within the PO2 limits given. In zone III, Pt greater than 50 ATA and PO2 greater than 0.2 ATA, tc is of the order of 2 min, and the seizures are essentially HPNS seizures only slightly modified by hyperoxia. The data are interpreted as suggesting that zone I represents hyperoxic seizures facilitated by high pressures, whereas zone II represents HPNS type I seizures facilitated by hyperoxia.
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PMID:Synergism of hyperoxia and high helium pressures in the causation of convulsions. 681 23


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