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

The authors examined the effects of large intravenous doses of sufentanil (5-160 micrograms/kg) on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) in rats. CBF and CMRO2 were measured by a modified Kety-Schmidt technique using 133Xenon washout. Progressive decreases in CBF and CMRO2 occurred in animals receiving sufentanil. The maximum decrease was 53% and 40% for CBF and CMRO2 respectively, at a dose of 80 micrograms/kg. The values for CBF and CMRO2 in this group were 105 +/- 10 ml X 100 g-1 X min-1 (mean +/- SEM) and 6.5 +/- 0.5 ml X 100 g-1 X min-1, respectively, compared with 226 +/- 28 ml X 100 g-1 X min-1 and 10.9 +/- 1 ml X 100 g-1 X min-1 in the control group, which received N2O 70% in oxygen. Larger doses of sufentanil did not cause further significant changes in CBF and CMRO2. Sharp waves appeared on the electroencephalogram (EEG) of all the animals following sufentanil injection, and some animals had EEG changes develop consistent with seizure activity. This seizure-like activity appeared to consist of a single episode of short duration in the groups receiving 5, 10, and 20 micrograms/kg sufentanil. The incidence and frequency of seizure activity increased in the groups receiving higher doses of sufentanil, although the duration of seizures was still short. The results of this study indicate that sufentanil causes a significant decrease in CBF and CMRO2 similar to that previously reported for fentanyl, and high doses of sufentanil may cause frequent seizure-like patterns appearing on EEG.
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PMID:Influence of sufentanil on cerebral metabolism and circulation in the rat. 316 29

Intermittent O2 breathing is a proven means of delaying pulmonary O2 toxicity during exposure to hyperbaric oxygen. The effect of an intermittent exposure in the pressure range toxic to the CNS was studied. Conscious, unrestrained rats, implanted with cortical EEG electrodes were subjected at 5 and 6 ATA to alternating periods of 7 min O2 and 7 or 10 min of either air, normoxic nitrox, or N2O-air (the latter mixture being equinarcotic to pure O2). Altogether, nearly half of the animals survived 90 min of intermittent breathing, with no grossly abnormal EEG patterns. At that time, labored breathing (associated with mild lung pathology) supervened. In the remaining animals, seizure patterns in the EEG appeared after a mean cumulative O2 breathing time of 20 min (compared to 9 min during a continuous exposure). Forty percent were affected while breathing the alternating mixture (low-PO2 seizures), mostly soon after switching of the gas. The nature of the alternating mixture did not affect the outcome of the high-PO2 seizures nor did the length of the interim periods. Normoxic nitrox increased and N2O-air reduced the incidence of low-PO2 seizures. At 5 ATA only 10% of the animals experienced high-PO2 seizures. While swift reversibility of the toxic process is indicated, the low-PO2 seizures with as yet an undetermined mechanism pose a serious obstacle for intermittent exposures at this pressure range.
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PMID:Central nervous system oxygen toxicity in the resting rat: postponement by intermittent oxygen exposure. 320 31

We studied the effect of inhaled anesthetic agents on the electrocorticogram (ECoG) in four epileptic patients during nondominant right hemisphere temporal lobectomy while they received 70% nitrous oxide in oxygen (70% N2O/O2) alone, 70% N2O/O2 with 0.5 to 1.5% isoflurane, or 70% N2O/O2 with 2% enflurane. The mean frequency of epileptiform spikes decreased during use of isoflurane, but not enflurane, compared with use of 70% N2O/O2 alone. Enflurane produced paroxysms of synchronous high-voltage spikes. The mean number of electrodes exhibiting spike activity decreased with isoflurane use and increased with enflurane use compared with use of 70% N2O/O2 alone. This preliminary study suggests that isoflurane can suppress epileptogenic tissue and that both isoflurane and enflurane can distort the ECoG, confounding accurate identification of the seizure focus. When used judiciously, however, enflurane may be a potent synchronizer and activator of the epileptogenic focus, making it easier to identify.
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PMID:Effect of isoflurane and enflurane on the electrocorticogram of epileptic patients. 336 75

Exposure of CD-1 mice to subanesthetic partial pressures of N2O (0.5 atm) or N2 (10-20 atm) for periods up to 14 days results in up to 40% decreases in the mean threshold pressure eliciting type I high-pressure neurological syndrome (HPNS) seizures, and in increases up to 38% in the N2 partial pressure producing anesthesia. For all combinations of preexposure time, N2 partial pressure, as well as identity of the conditioning gas the relations between the convulsion threshold pressure (Pc) and the anesthesia N2 pressure (Pa) appear to be uniquely correlated by the equation Pa = 54.5 - 0.2(Pc - 60)1.2. The potency of N2O with respect to these habituation phenomena is between 28 and 33 times higher than that of N2, depending on the aspects compared. Evidence is presented indicating that after 14 days of habituation the animals have attained between 75 and 85% compensation for the anesthetic as well as the anticonvulsant effects of the conditioning gas. The bearing of the results on the problem of the nature of the antagonism between inert gas narcotic agents and high pressure and on the hypothesis that habituation tends toward restoration of isofluidity (or some analogous normalization process) are discussed.
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PMID:Effect of habituation to subanesthetic N2 or N2O levels on pressure and anesthesia tolerance. 355 2

Cerebral partial pressure of O2 (PO2), relative changes in the ratio of reduced/oxidized cytochrome aa3, blood flow, and the arteriovenous difference in O2 content were measured during seizures with and without pulmonary edema. Seizures were induced with bicuculline (0.2-1.2 mg/kg iv) in rats anesthetized with 70% N2O and paralyzed with curare. Briefer seizures were accompanied by increased cerebral PO2 and increased oxidation of cytochrome aa3. Lung water content and arterial O2 partial pressure (PaO2) remained normal. Longer duration seizures were also accompanied initially by increases in cerebral oxygenation. Within minutes, however, PaO2 fell from a mean of 118 to 51 mmHg, and lung water content increased from 76.2 to 83.6%. Cerebral PO2 fell but most often rose back to or above control levels, while cytochrome aa3 became markedly reduced. Simultaneously, cerebral blood flow increased more than 300% above preseizure values and O2 delivery increased more than O2 consumption. The reductive shift of cytochrome aa3 was greater than that produced by lowering PaO2 to equivalent values in seizure-free rats. The reductive shift of cytochrome aa3, despite increased O2 delivery, may be indicative of derangements in cerebral O2 diffusion or energy metabolism.
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PMID:Seizure-associated pulmonary edema and cerebral oxygenation in the rat. 355 25

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

Twenty generations of selective breeding were used to produce lines (strains) of mice which differ markedly from one another in ethanol physical dependence development as indexed by handling-induced convulsions (HIC) induced by withdrawal from ethanol. These withdrawal seizure prone (WSP) and withdrawal seizure resistant (WSR) selection lines now differ by over 10-fold in HIC scores after equivalent exposure to intoxicating levels of ethanol via inhalation. Since handling-induced convulsions can be readily elicited following withdrawal from nitrous oxide, we sought to determine if the very large differences in ethanol withdrawal-induced HIC bred into these selection lines would generalize to nitrous oxide. Following a 60 min exposure to 75% nitrous oxide (in O2), a greater than 10-fold difference in HIC scores, and a 2-fold difference in tremor incidence was seen upon withdrawal in WSP vs. WSR mice. These findings closely parallel those seen with ethanol, and demonstrate that a large degree of commonality exists in the genes and the mechanisms determining these withdrawal signs. HIC elicited by nitrous oxide withdrawal were readily suppressed by ethanol, and HIC elicited by ethanol withdrawal were promptly suppressed by 75% nitrous oxide in WSP mice. Nitrous oxide also suppressed HIC and tremor associated with nitrous oxide withdrawal.
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PMID:Ethanol and nitrous oxide produce withdrawal-induced convulsions by similar mechanisms in mice. 366 9

Fentanyl reduces the cortical cerebral blood flow and metabolic rate for oxygen in rats, though seizure activity occurs in some animals at high doses. However, the effects of fentanyl on blood flow and metabolism in subcortical structures have not been clearly delineated. The present study examines the effects of intravenous fentanyl (100 or 400 micrograms . kg-1) on local cerebral blood flow (1-CBF) in paralyzed, mechanically ventilated rats. Rats ventilated with 70% N2O in 30% O2 served as controls. Local CBF was measured using 14C-iodoantipyrine and autoradiography. Blood pressure, PaO2, PaCO2, pH, and temperature were comparable in all groups. The EEG showed slow wave activity in most animals given 100 micrograms . kg-1 fentanyl while seizure activity occurred in all animals given 400 micrograms . kg-1 fentanyl. With 100 micrograms . kg-1 fentanyl, CBF tended to be depressed in all cortical and subcortical areas, except the peri-aqueductal gray; and with 400 micrograms . kg-1 fentanyl, 1-CBF tended to be elevated (compared to 100 micrograms . kg-1 fentanyl) in most areas of the brain. The limbic system structures, however, were most affected by 400 micrograms . kg-1 fentanyl with statistically significant increases (compared to the 100 micrograms . kg-1 group) in 1-CBF of 86% and 67% respectively in the amygdala and septal nucleus. These results confirm that moderately high doses of fentanyl which cause slow wave activity on the EEG also depress 1-CBF in rats; moreover, doses of fentanyl that produce seizure activity produce increases in 1-CBF in most cerebral structures with greatest effects on limbic system 1-CBF.
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PMID:Effects of fentanyl on local cerebral blood flow in the rat. 406 Oct 1

The objective of the present study was to explore if lesions of the ascending noradrenergic pathways, originating in the locus coeruleus, modulate the cerebral metabolic response to bicuculline-induced seizures in rats. Bilateral noradrenergic lesions were performed by 6-hydroxydopamine injections in the caudal mesencephalon, 12-22 days before seizures were induced in animals ventilated on N2O:O2 (75:25). After 5 min of seizures the brain was frozen in situ and cerebral cortex and hippocampus were sampled for analysis. Labile phosphates, glycolytic metabolites, cyclic nucleotides, and free fatty acids were measured. In another series, lesioned animals were used for measurements of cerebral oxygen consumption. The noradrenergic lesions neither modified the electroencephalographically recorded seizure discharge, nor did they alter cerebral oxygen consumption or cerebral energy state. However, when compared to sham-operated animals, those with noradrenergic lesions had significantly higher (115% and 68%) glycogen concentrations and lower (50% and 52%) cyclic AMP concentrations in cerebral cortex and hippocampus, respectively, demonstrating the marked influence of noradrenergic activity on adenylate cyclase activity and glycogenolysis. The lesions failed to modulate the rise in free fatty acids in the cerebral cortex, or the cyclic GMP concentrations in the cerebral cortex and hippocampus. Thus, increased noradrenergic activity during status epilepticus does not seem responsible for lipolysis or for activation of guanylate cyclase.
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PMID:Influence of lesions of the noradrenergic locus coeruleus system on the cerebral metabolic response to bicuculline-induced seizures. 630 1

A model is described in which transient ischemia is induced in rats anaesthetized with N2O:O2 (70:30) by bilateral carotid artery clamping combined with a lowering of mean arterial blood pressure to 50 mm Hg, the latter being achieved by bleeding, or by bleeding supplemented with administration of trimetaphan or phentolamine. By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long-term recovery studies. Autoradiographic measurements of local CBF showed that the procedure reduced CBF in neocortical areas, hippocampus, and caudoputamen to near-zero values, flow rates in a number of subcortical areas being variable. Administration of trimethaphane or phentolamine did not affect ischemic and postischemic flow rates, nor did they alter recovery of EEG and sensory-evoked responses, but trimetaphan blunted the changes in plasma concentrations of adrenaline and noradrenaline. Recovery experiments showed that 10 min of ischemia gave rise to clear signs of permanent brain damage, with a small number of animals developing postischemic seizures that led to the death of the animals in status epilepticus. After 15 min of ischemia, such alterations were more pronounced, and the majority of animals died. It is concluded that the short revival times noted are explained by the fact that the model induces near-complete ischemia, and that recovery following forebrain ischemia is critically dependent on residual flow rates during the period of ischemia.
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PMID:Models for studying long-term recovery following forebrain ischemia in the rat. 2. A 2-vessel occlusion model. 646 70


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