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

Cerebral blood flow (CBF) and cerebral metablic rate for oxygen (CMRO2) have been studied during sustained epileptic seizures induced by bicuculline (1-2 mg/kg, i.v.) in paralysed Wistar rats, artificially ventilated with nitrous oxide/oxygen. CBF was determined by venous outflow collection, and by 133Xe desaturation, using sagittal sinus blood (for cerebral cortical flow) or retroglenoid venous blood (for 'whole brain' flow). The procedure employed ensured that arterial oxygenation remained normal and blood glucose concentration was normal or high throughout the seizure. Arterial hypotension was prevented by the infusion of donor blood. CBF increased concurrently with seizure onset, reaching a maximum nine times higher than control value after 15-60 s. This was due to a marked rise in mean arterial pressure (to greater than 180 torr) and a dramatic fall in cerebrovascular resistance to less than 15 per cent of control). Subsequently, with decreasing blood pressure, CBF slowly diminished, being more than four times higher than control at 20 min, and slightly less than three times higher than control at two hours. The different procedures for measuring CBF gave closely similar results. A threefold increase relative to control CMRO2 (7-6 ml/100 g-1/min-1 for 'whole brain,' and 10-2 ml/100 g-1/min-1 for cerebral cortex) was measured after 1-20 min of seizure activity (utilizing either the venous outflow or the 133Xe desaturation procedure for CBF determination). After two hours of seizure activity CMR02 was still more than twice as high as the control. This high metabolic rate during sustained seizure activity will increase the susceptibility of the brain to 'ischaemic' damage during prolonged seizures in man in which an additional metabolic stress may be imposed by cerebral hypoxia, arterial hypotension, hyperpyrexia or hypoglycaemia.
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PMID:Cerebral blood flow and metabolic rate early and late in prolonged epileptic seizures induced in rats by bicuculline. 100 Feb 85

Changes in cardiodynamics and regional blood flow were examined in chronically prepared paralyzed cats during seizures induced electrically by transcerebral or direct cortical stimulation or by administration of flurothyl ether (Indoklon) or pentylenetetrazol (Metrazol). Transcerebral and chemical stimuli produced the greatest vascular responses. During seizures there was an abrupt elevation of arterial pressure unassociated with consistent changes in heart rate. Vascular resistance was increased in femoral, renal and mesenteric arteries with variable reductions in blood flow. Resistance was decreased and flow passively increased in the common carotid artery reflecting the loss of cerebral autoregulation. Cardiac output was unchanged. With seizures associated with large elevations of arterial pressure, the central venous and left ventricular end-diastolic pressures were markedly increased indicating incipient congestive failure. The pressor response was blocked by alpha-adrenergic blockade with phentolamine. Increased regional vascular resistance was abolished by regional sympathectomy. While either adrenalectomy or treatment with 6-hydroxydopamine alone failed to abolish the pressor response, combined, they did. Such treatment unmasked an atropine-sensitive bradycardia. The pressor response with seizures is a consequence of increased vascular resistance in viscera and muscles due to widespread activation of sympathetic neurons and release of adrenomedullary catecholamines. Co-activation of cardiovagal and cardiosympathetic neurons may underlie some associated arrhythmias. Cardiovascular events may severe, by redistribution of the cardiac output, to assure increased availability of oxygen and nutrients to brain to meet the metabolic demands of convulsions.
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PMID:Changes in regional blood flow and cardiodynamics associated with electrically and chemically induced epilepsy in cat. 113 82

Several aryl and heteroaryl hydrazides were synthesized and evaluated for their inhibitory effects on glutamic acid decarboxylase (GAD), GABA-alpha-oxoglutarate aminotransferase (GABA-T), and monoamine oxidase (MAO) enzyme systems in chick brain 24 h after their intramuscular administration (0.75 mmol/kg). All compounds produced a reduction in GAD, GABA-T, and MAO activity. Structure-activity relationships indicated that the ring structure had a greater influence on the degree of GAD and GABA-T inhibition than did the N'-terminal group. In contrast, structural requirements for MAO inhibition were much more restrictive. The intramuscular administration of benzoic acid hydrazide to chicks 24 h prior to their being exposed to oxygen at high pressure provided significant protection against the onset of the hyperbaric oxygen-induced seizures.
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PMID:Molecular structure--activity relationship of hydrazides inhibiting glutamic acid decarboxylase, GABA-alpha-oxoglutarate aminotransferase, and monoamine oxidase activities in chick brain. 113 48

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

The effect of sodium cyanate (25, 50, 75, and 100 mg/kg body weight i.p. daily for 10 days) upon cerebral metabolism and the EEG of Wistar rats was studied. This treatment resulted in a dose-related carbamylation of hemoglobin and left shift in the oxygen dissociation curve. Animals receiving the highest dose of cyanate developed a significant systemic metabolic acidosis. In brain there was dose-dependent decrease in phosphocreatine, TCO2 and cytoplasmic NADH/NAD+ ratio, reflecting the calculated drop in intracellular pH. Glucose levels were elevated despite a normal calculated energy charge, which suggests a balanced slowing of the energy-producing and energy-utilizing systems. The higher doses of cyanate produced spontaneous seizure activity on the EEG.
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PMID:Effects of high-dose cyanate upon cerebral energy metabolism of the rat. 120 41

The advantages of a bloodless field and total cardiac relaxation have popularized the technique of deep hypothermia and total circulatory arrest for the correction of complex congenital cardiac defects in infancy. There is, however, a significant potential for cerebral and pulmonary complications. Presently, the most common technique is that of using a combination of surface cooling and cardiopulmonary bypass cooling and rewarming. Normal neurological development has been claimed with the present technique of hypothermia at 20 degrees C and total circulatory arrest for periods up to an hour; however, there are reports of seizure activity in the early postoperative period. There is also a disturbing incidence of respiratory insufficiency and, occasionally, hemorrhagic pulmonary edema. This study, using growing puppies and subjecting them to deep hypothermia and total circulatory arrest for varying periods of time, disclosed that animals subjected to 60 min of circulatory arrest recovered neurologically; however, there were histological changes of anoxia in the brain. Animals subjected to 30 min of total circulatory arrest were normal neurologically and there was no histological evidence of anoxic damage to brain tissue. Puppies that were continuously on cardiopulmonary bypass had no significant pulmonary changes caused by increasing the inspired oxygen tension in the ventilator; however, striking changes were noted when limited cardiopulmonary bypass was employed for core cooling and total circulatory arrest combined with pulmonary ventilation with 100% oxygen. We conclude from this experimental study that the use of surface cooling and core cooling with subsequent total circulatory arrest at 20 degrees C is a safe procedure, providing the period of time of cardiac arrest is kept around 30 min. We also conclude that the alveolar oxygen tension should be maintained at the lowest level possible during the interval of circulatory arrest to avoid the apparent rapid onset of post-traumatic pulmonary insufficiency.
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PMID:Effect of deep hypothermia, limited cardiopulmonary bypass, and total arrest on growing puppies. 120 92

Continuous electroencephalographic recordings were taken in 25 children who had ethrane-nitrous oxide anaesthesia without a basal anaesthetic. The recordings confirmed the repeatedly reported occurrence of certain abnormal wave patterns distinctive of seizures during ethrane anaesthesia. Although these dysrhythmias were more frequent and more pronounced at higher ethrane concentrations and during hyperventilation, sharp spikes began to appear already at concentrations of 1.0/p.c. without hyperventilation and at moderate depths of anaesthesia. In no case did the usual criteria for assessing depth of anaesthesia provide an indication of over-dosage. Although in the individual case there was a close relationship between the concentration of ethrane in the inhaled mixture and the electroencephalographic changes, the differences between the cases were too great to allow any prediction as to the concentration of ethrane that would bring on the dysrhythmia. Considering that increased cerebral oxygen consumption has been observed to accompany the abnormal wave patterns ethrane is not recommended for use in epileptic children or those with a familial history of epilepsy.
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PMID:[Electroencephalographic changes during ethrane anaesthesia in children (author's transl)]. 123 78

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

Although reactive O2 species appear to participate in central nervous system (CNS) O2 toxicity, the exact roles of different reactive O2 species are undetermined. To study the contribution of extracellular superoxide anion (O2-) to CNS O2 toxicity we constructed transgenic mice overexpressing human extracellular superoxide dismutase (ECSOD; superoxide:superoxide oxidoreductase, EC 1.15.1.1) in the brain. Remarkably, when exposed to 6 atm (1 atm = 101.3 kPA) of hyperbaric oxygen for 25 min, transgenic mice demonstrated higher mortality (83%) than nontransgenic litter-mates (33%; P < 0.017). Pretreatment with diethyldithiocarbamate, which inhibits both ECSOD and Cu/Zn superoxide dismutase (Cu/Zn SOD) activity, increased resistance to CNS O2 toxicity, in terms of both survival (100% in transgenics and 93% in nontransgenics) and resistance to seizures (4-fold increase in seizure latency in both transgenic and nontransgenic mice; P < 0.05). Thus, O2- apparently protects against CNS O2 toxicity. We hypothesized that O2- decreased toxicity by inactivating nitric oxide (NO.). To test this, we inhibited NO. synthase (EC 1.14.23) with N omega-nitro-L-arginine to determine whether NO. contributes to enhanced CNS O2 toxicity in transgenic mice. N omega-nitro-L-arginine protected both transgenic and nontransgenic mice against CNS O2 toxicity (100% survival and a 4-fold delay in time to first seizure; P < 0.05), as well as abolishing the difference in sensitivity to CNS O2 toxicity between transgenic and nontransgenic mice. These results implicate NO. as an important mediator in CNS O2 toxicity and suggest that ECSOD increases CNS O2 toxicity by inhibiting O2(-)-mediated inactivation of NO.
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PMID:Extracellular superoxide dismutase, nitric oxide, and central nervous system O2 toxicity. 132 5

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


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