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

This study compares the effects of various so-called trimix mixtures (10, 20, and 40% N2 in He-O2) on the convulsion threshold pressure (Pc) and EEG activity in 60 adult male Wistar rats with chronically implanted electrodes with those in 20 rats in He-O2 only. Restrained animals were individually compressed with trimix mixtures at 80 or 160 atm per hour to a simulated depth of 138 ATA; colonic temperature was maintained at normal levels. Pc was defined as the initial occurrence of overt sustained generalized tonic-clonic seizures, accompanied by typical "spike and wave" patterns in all EEG leads. As in man, in rats trimix increased the depth of the onset of HPNS tremors and myoclonic jerks in all six groups of rats. However, the Pc of the trimix groups was no different from the Pc of the helium-oxygen group (113 ATA), and at 40% N2, rats showed EEG seizures but no overt convulsions. These results are discussed in relation to those of other studies showing the extension of Pc in mice and monkeys attained by adding narcotics to heliox; the paper also considers the relevance of method of compression, addition of nitrogen, core temperature, and species differences, as well as the need for EEG measurements and direct observation of overt convulsions as indicators of an effective antagonism of HPNS.
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PMID:Effect of helium/nitrogen/oxygen mixtures on HPNS convulsion threshold in euthermic rats. 53 65

To evaluate the interaction between high pressure nervous syndrome (HPNS) seizures and cerebellar integrity, seizure threshold pressure (Pc) of normal rats was compared with that of rats sustaining cerebellar ablation two weeks prior to exposure to 136 ATA in a helium-oxygen atmosphere. All rats exhibited severe HPNS symptoms which culminated in seizures. Pc was reduced in cerebellectomized animals, and the number of seizure episodes increased twofold, but the average duration of seizure episodes was unchanged. The spike-and-wave pattern in the electroencephalogram remained a prominent feature in both groups.
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PMID:Effect of cerebellar ablation on the high pressure nervous syndrome in rats. 63 75

A variety of autonomic blocking agents, general anesthetics, and anticonvulsants have been shown to offer protection from seizures caused by hyperbaric oxygen. Amino-oxyacetic acid (AOAA) has been shown to offer rats only minimal protection from such seizures. This study investigated whether AOAA protected cats and mice from hyperbaric-oxygen-induced seizures. Cats and mice were exposed to 100% oxygen at 5 ATA until seizures occurred or for a period of up to 60 min. Approximately half of the animals were pretreated with AOAA either 30 or 240 min before oxygen exposure. Results showed that the interval between exposure and grand mal seizures increased significantly in cats pretreated 30 or 240 min before exposure with 17 to 25 mg/kg AOAA; the number of cats remaining seizure-free for 60 min also increased markedly. However, mice received little protection even at doses up to 40 mg/kg. At higher doses the AOAA itself caused seizures even in the absence of hyperbaric oxygen.
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PMID:Protection against high-pressure oxygen seizures by amino-oxyacetic acid. 70 42

Prolonged exposure to hyperbaric O2 (HBO) causes seizures and eventual death. The precise molecular basis for O2 toxicity is not known but may be due to increased biological production of superoxide anion (O2-). In the present study, superoxide dismutase (SOD), an enzyme that catalyzes the dismutation of O2- to less toxic forms, was evaluated for its ability to protect against HBO-induced seizures and death, and the results were compared to those concurrently obtained with succinate (SUCC), an agent previously reported to protect against HBO-induced seizures. Preconvulsion time and survival time in normal and vitamin E-deficient rats exposed to 100% O2 at 5 ATA were not significantly prolonged by pretreatment with 2 to 20 mg/kg SOD intraperitoneally (ip) or 0.1 to 1.0 mg/kg SOD intrathecally. In contrast, 12 mmol/kg SUCC ip significantly prolonged preconvulsion time in normal and vitamin E-deficient rats and survival time in normal rats. The ability of SUCC to stimulate ATP production may account for its protective role. Reasons for the failure of SOD to protect against O2 toxicity are discussed.
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PMID:Effect of superoxide dismutase and succinate on the development of hyperbaric oxygen toxicity. 88 36

Homogenates were prepared from the basal ganglia and frontal cortex of human brain and incubated for 20 min of 25 degrees C under either 1 ATA N2 or 3 ATA O2 (OHP). Exposure of the homogenates to OHP caused a significant inhibition in the activity of the gamma-aminobutyric acid (GABA) synthesising enzyme, glutamic acid decarboxylase. This finding, together with previously published data on animal experiments, suggests that a deranged GABA metabolism must be given serious consideration as a possible mechanism for OHP-induced seizures in man.
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PMID:Sensitivity of GABA synthesis in human brain to oxygen poisoning. 116 54

Previous work has shown that short-term exposure of cats to oxygen at high pressure (OHP), to the extent of overt convulsive seizures, has little or no effect on the lung appearance or lung weight but does alter the alveolar surfactants. More prolonged exposure results in hemorrhagic edema of the cat lung similar to that observed in rats after only short-term exposure. Previous work showed that sympathetic stimulation via the stellate ganglion and mechanical CNS injury results in altered surfactants attributed to increased intra-alveolar cholesterol. In the present study, cats exposed to OHP until the animals convulsed intermittently for 3 min (approximately 1 hour, 6 ATA) similarly showed altered surfactants with a high minimum surface tension and a 150% increase in intra-alveolar cholesterol. These changes also occurred in the absence of any gross lung injury. The results from the present study suggest that an important causal mechanism involved in the development of gross lung injury associated with prolonged OHP exposure is an initial increase in minimum surface tension due to increased intra-alveolar cholesterol.
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PMID:Hyperbaric oxygen and pulmonary surface tension. 117 14

This paper reports the effect of acupuncturing "Renzhong" (GV26) and "Chengjiang" (GV24) points on OHP*-induced convulsion in mice. The results are as follows: 1. Convulsion induced by 6 ATA OHP were accompanied with a decrease in the brain GABA concentration. 2. When electro-acupuncture was applied for 15 minutes prior to exposure to hyperoxic chamber, the latency of convulsions was lengthened and the symptoms of seizures were alleviated. Besides, the brain GABA concentration was also elevated remarkably. 3. Administration of vitamin B6 enhanced the effect of acupuncture on convulsions and increased brain GABA concentration. 4. The latency of convulsions was well correlated with the GABA concentration of the brain (r = 0.9867). The above results indicate that acupuncture may elevate endogenous GABA levels in the brain and prevent the hyperbaric-oxygen-induced the decrease in the brain GABA content. Therefore. It is of protective effect against oxygen convulsions. Vitamin B6 may facilitate the effect of acupuncture by improving the GABA metabolism in the brain. In short, the effect of acupuncture against oxygen convulsions may be closely related to the increase in the brain GABA levels.
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PMID:[The effect of acupuncture on high oxygen pressure-induced convulsion and its relationship to the brain GABA concentration in mice]. 128 20

Under continuous compression with normoxic helium-oxygen mixture up to 100 Ata with the velocity 1 Ata/min, guinea pigs developed successively tremor, myoclonias, seizures of clonic and tonic types. Blood supply of cerebral structures (cortex, black substance, caudate nucleus) during motor disorders increased depending on the stage of development of the high pressure neural syndrome. The role of cerebral circulation in the latter's pathogenesis is discussed.
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PMID:[The local blood supply of the brain in guinea pigs during the development of the high-pressure nervous syndrome]. 133 Jul 49

Changes in amino acids (AA) and ammonia were investigated in the cerebral cortex and striatum of rats after the following conditions: 1) one hyperbaric oxygen (HBO)-induced seizure (6 ATA O2); 2) exposure to 6 ATA air; and 3) exposure to atmospheric pressure (no seizures in both latter groups). Exposure to 6 ATA air produced no change with respect to atmospheric pressure. After HBO seizure, AA levels (except for gamma-amino butyric acid, GABA, and glutamine), with respect to 6 ATA air levels, were altered in the striatum with a concomitant rise in ammonia (+70%) at variance with the cortex. These changes could be explained by increased oxidative deamination in the striatum. Decrease in taurine content (-66%) in the striatum, where HBO lipoperoxidation exists, suggests an alteration of glial function leading to blockade of uptake and loss of released products in interstitial fluid. This pattern of change recalls the one seen in ischemic conditions, but cannot be confirmed in the absence of measurements of extracellular amino acid levels under HBO conditions. The maintenance in the level of GABA would favor its role in controlling seizure. In the cortex, only a few AA levels decreased, along with a nonsignificant trend for ammonia to increase. The remaining abnormalities in the striatum, after the first HBO seizure, may explain the already known repetition of seizures in continuously exposed animals and are consistent with previous data on the important role of the striatum.
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PMID:Changes in striatal and cortical amino acid and ammonia levels of rat brain after one hyperbaric oxygen-induced seizure. 161 Mar 39

To explore the role of glutathione in protecting rats from hyperbaric hyperoxia, we administered buthionine sulfoximine (BSO) to block gamma-glutamyl cysteine synthase activity and decrease tissue glutathione synthesis. We then exposed these animals and their vehicle-treated matched controls to 100% oxygen at 4 ATA or room air at 1 ATA. After BSO treatment, glutathione concentrations in air-exposed controls decreased 62% in lung, 76% in liver, 28% in brain, and 62% in plasma. Paradoxically, BSO-treated rats were protected from hyperbaric hyperoxia. The BSO-treated animals seized significantly later and had a markedly prolonged time of survival compared with the vehicle-treated controls. We conclude that BSO treatment protects rats from hyperbaric hyperoxia, despite its effects of lowering plasma and tissue glutathione concentrations. This protection may be related to a direct effect of the compound in decreasing free radical-mediated tissue injury, increasing tissue antioxidant defenses, or increasing seizure threshold.
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PMID:Protection from hyperbaric oxidant stress by administration of buthionine sulfoximine. 168 Aug 46


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