Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the efficacy of pretreatment with phenytoin and phenobarbital to prevent seizures in mice given convulsive doses of theophylline. The control LD50 for theophylline was determined in 48 mice by intraperitoneal injections of increasing doses without anticonvulsant treatment. Anticonvulsant effects were determined in 105 additional mice pretreated with either phenytoin 30 mg/kg (n = 35), phenobarbital 35 mg/kg (n = 30), or phenobarbital 60 mg/kg (n = 40) one hour before theophylline administration. The theophylline LD50 (95% confidence interval) was 239 mg/kg (range, 229 to 248 mg/kg) for controls, 204 mg/kg (range, 194 to 214 mg/kg) for phenytoin, 305 mg/kg (range, 288 to 323 mg/kg) for low-dose phenobarbital, and 319 mg/kg (range, 307 to 331 mg/kg) for high-dose phenobarbital. Each LD50 differed significantly from control (P less than .05). The phenobarbital groups were significantly different from phenytoin (P less than .05) but not from each other. Theophylline serum concentrations were not significantly different among groups after adjustment for different doses. The mean +/- SEM time to seizure in minutes after adjustment for theophylline dose was 23.5 +/- 4.0 minutes for controls, 5.7 +/- 7.5 minutes for phenytoin, 44.1 +/- 7.1 minutes for low-dose phenobarbital, and 63.7 +/- 6.5 minutes for high-dose phenobarbital.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relative efficacy of phenytoin and phenobarbital for the prevention of theophylline-induced seizures in mice. 317 89

Of 33 infants with hypernatremic dehydration (serum Na+ of greater than or equal to 150 mEq/L) 7 were excluded, 6 because severe alteration of the level of consciousness or shock precluded oral rehydration and 1 because he was given glucose-electrolyte solution plus water. We studied the remaining 27 infants. Twenty (group A) were treated with the World Health Organization-recommended oral rehydration solution (90 mEq/L Na+) and seven (group B) were treated with Pedialyte-RS (Abbott Laboratories Ltd.; 75 mEq/L Na+). The rehydrating solutions were administered in a volume equivalent to twice the clinically estimated fluid deficit. Initial serum sodium was 156.7 +/- 0.9 mEq/L for group A and 155.8 +/- 1.8 mEq/L for group B (mean +/- SEM). The mean time to achieve rehydration was 14.3 and 16.6 h for groups A and B, respectively. Twenty-four hours after commencing oral rehydration, serum Na+ had decreased to 144.8 +/- 1.8 mEq/L for group A and 144.5 +/- 0.9 mEq/L for group B. In two patients in group A, the serum Na+, which, had not decreased to less than 150 mEq/L at 24 h, did so at 48 h. Only in one case (group A) did the serum Na+ increase. This patient had high stool output and failed to become rehydrated after 24 h of unsuccessful oral rehydration. None of the patients had seizures or persistent CNS dysfunction. We conclude that the slow administration of oral rehydration solutions containing either 90 or 75 mEq/L Na+ is a safe and effective treatment of hypernatremic dehydration.
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PMID:Hypernatremic diarrheal dehydration treated with oral glucose-electrolyte solution containing 90 or 75 mEq/L of sodium. 318 73

Generalized seizures may be associated with therapeutic or intentional theophylline overdose. Toxic levels of theophylline are also associated with a fall in potassium which could potentiate theophylline-induced seizures. To evaluate the role of serum potassium concentration in theophylline-induced seizures we investigated the seizure threshold in normokalemic and hyperkalemic rats during theophylline infusion to toxic levels. Hyperkalemic rats were prepared with intraperitoneal amiloride and potassium chloride and had a mean +/- SEM initial potassium of 5.29 +/- 0.15 mEq/L. Control animals received either amiloride or potassium and had initial serum potassium concentrations of 4.00 +/- 0.08 and 3.93 +/- 0.16 mEq/L, respectively. Potassium levels after 30 minutes of theophylline infusion were 4.11 +/- 0.18 mEq/L in the hyperkalemic rats and 3.47 +/- 0.06 and 3.51 +/- 0.12 mEq/L in the control animals. There were no significant differences in the serum theophylline concentrations at time of seizure, nor was there a correlation between serum potassium concentration and theophylline concentration at time of seizure. Since the preservation of normokalemia does not influence the onset of seizures in theophylline toxicity, this suggests that the potassium level has little effect on seizure activity in this model.
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PMID:The effect of serum potassium on theophylline-induced seizures. 318 59

A controlled study was conducted to quantitate plasma catecholamines in magnesium-deficient weanling rats experiencing the seizure-shock episode. Eighty-four male Sprague-Dawley rats each weighing 35.6 +/- 0.3 g (mean +/- SEM) were fed purified diets to which was added 150 mg magnesium/100 g (Mg-150) or no magnesium (Mg-0). Studies were conducted between d 5 and 8. Plasma and bone magnesium and calcium were measured by atomic absorption spectrophotometry, and plasma catecholamines by radioenzymatic assay using 3H. Compared with Mg-150 rats, the Mg-0 rats showed reduced weight gain (P less than 0.001); reduced plasma magnesium (P less than 0.001) and reduced bone magnesium (P less than 0.001) with no corresponding changes in calcium concentration; and a 25% mortality by d 8. Pair-feeding and 80-dB noise provoked no changes in plasma catecholamines in Mg-150 rats, but both strychnine-induced seizures in Mg-150 rats and seizures induced by 80-dB noise in Mg-0 rats were accompanied by massive increases in plasma catecholamines. In contrast, 80-dB noise in Mg-0 provoked a massive increase in plasma catecholamines (P less than 0.001). However, gross pulmonary pathology developed only in Mg-0-shocked rats, not Mg-150-shocked animals. The study provides no evidence for a role of catecholamines in the pathogenesis of Mg-0 shock. The weanling rat displayed the ability to release massive quantities of three catecholamines during the final stages of acute magnesium deficiency and to normalize the plasma catecholamine levels within 16 h after seizure shock.
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PMID:Plasma catecholamines in acute magnesium deficiency in weanling rats. 377 20

We reviewed clinical data in 33 patients with transient hyperammonemia of the newborn (THAN): six previously unreported cases and 27 from the literature. Thirteen neonates with urea cycle enzyme deficiencies (UCED) served for comparison. No differences were found in the incidence of perinatal complications, route of delivery, Apgar scores, sex, or incidence or time of onset of seizures. On the other hand, neonates with THAN had significantly lower birth weights (mean +/- SEM 2282 +/- 78 gm vs 3336 +/- 222 gm, P less than 0.001) and gestational ages (35.1 +/- 0.5 weeks vs 39.6 +/- 0.5 weeks, P less than 0.001). Mean time of onset of respiratory distress (3.9 +/- 1.4 hours vs 71.5 +/- 26.1 hours, P less than 0.001), ventilatory support (P less than 0.001), lethargy (P less than 0.005), and coma (P less than 0.005) occurred earlier in THAN. Distinctive laboratory findings in patients with THAN included abnormal chest radiographic findings and plasma ammonium concentrations that were higher (1871 +/- 209 microM vs 973 +/- 169 microM, P less than 0.02) at an earlier age. Respiratory distress occurred in all but one patient with THAN before 24 hours; in contrast, only 62% of infants with UCED had respiratory symptoms, and none before 30 hours. In this retrospective study, the clinical presentation alone differentiated THAN from UCED.
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PMID:Differentiation of transient hyperammonemia of the newborn and urea cycle enzyme defects by clinical presentation. 405 69

Twelve newborn infants were given morphine intravenously for postoperative analgesia. They received a continuous infusion of 6.2 to 40 micrograms/kg/hr for 9 to 105 hours (mean +/- SEM 59.5 +/- 10.2 hours); in four the infusion was preceded by a loading dose of 50 to 100 micrograms/kg. Morphine plasma concentrations correlated with the rate of infusion, but with large variability. There was a tendency for plasma morphine concentrations to decrease in some patients receiving a constant infusion rate, suggesting improvement in morphine clearance rate. Elimination half-life of morphine (13.9 +/- 6.4 hours) was significantly longer than in older children and adults (about 2 hours). Similarly, morphine concentrations in neonates receiving 20 micrograms/kg/hr for 24 hours were three times higher (52 +/- 31 ng/ml) than in older children receiving the same schedule. Two infants who received 32 and 40 micrograms/kg/hr, respectively, developed generalized seizures. Because of the apparently greater sensitivity to morphine and the lower elimination rate in newborn infants, the infused dose should not exceed 15 micrograms/kg/hr.
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PMID:Postoperative morphine infusion in newborn infants: assessment of disposition characteristics and safety. 406 57

The influence of hyperkalemia on the central nervous system and cardiac toxicity of bupivacaine and lidocaine was studied in open-chested mechanically ventilated dogs. The seizure and cardiotoxic doses of intravenously administered lidocaine and bupivacaine were determined in two separate groups of normokalemic (2.7 +/- 0.05 SEM mEq/1) dogs. In the case of both anesthetics, the cardiotoxic dose was found to be approximately four times the seizure dose. Under conditions of hyperkalemia (5.4 +/- 0.08 SEM mEq/1), however, the cardiotoxic doses of both anesthetics were decreased significantly to approximately two times the seizure dose. Hyperkalemia did not change the seizure dose for either anesthetic. The cardiac to seizure dose ratio was decreased significantly for bupivacaine but not for lidocaine. The results of this study suggest that hyperkalemia enhances the cardiotoxic effects of both lidocaine and bupivacaine, with this enhancement being more pronounced in the case of bupivacaine.
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PMID:The influence of serum potassium on the cerebral and cardiac toxicity of bupivacaine and lidocaine. 646 96

To define the utility of high-dose barbiturate therapy following an episode of complete global cerebral ischemia, we investigate the effects of 60 mg/kg of thiopental given to cats five minutes after resuscitation from 12, 14, or 16 min of electrically induced ventricular fibrillation (VF). All aspects of the arrest, resuscitation, with post-arrest care were carefully controlled, with the EEG becoming isoelectric 20-25 s after the onset mean resuscitation time of 2.5 +/- 0.2 (SEM) min. For any given duration of VF, there were no differences (control vs thiopental) in any pre- or post-arrest parameters (blood pressure, blood gases, electrolytes, etc.) A total of 68 resuscitated cats were entered into various treatment and control groups, and all but one group received 20-24 h of post-resuscitation paralysis, mechanical ventilation, and ICU support before being extubated. Cats received an additional six days of aggressive nursing care, and daily examinations were performed with the assignment of a neurologic deficit score (NDS) between 0 (normal) and (brain dead). Autopsies were performed to determine the cause of death in animals which died before the end of the seven-day observation period. The early post-arrest period was marked by the occurrence of repetitive, rhythmic bursts of high-frequency electroencephalographic (EEG) activity (? seizures) in 38 per cent of control animals (16/42, all arrest times combined). Ten of these animals died as a result of severe neurologic injuries. By contrast, only 12 per cent of treated cats (3/26) developed similar EEG patterns (P less than 0.05) and there were no neurologic deaths in the thiopental groups. The differences in the incidence of neurologic deaths (control vs. thiopental) was significant (P less than 0.02). The change in overall mortality did not quite reach significance (36 per cent vs. 21 per cent), and treatment had no effect on the incidence of deaths due to cardiovascular causes (e.g., myocardial infarctions). In spite of the effects on mortality, treatment had no effect on the neurologic function of survivors (assessed by NDS). These findings suggest that thiopental improved survival rates by suppressing an unusual post-arrest EEG pattern (? anticonvulsant effect), but had no additional cerebral protective effects.
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PMID:The neurologic effects of thiopental therapy following experimental cardiac arrest in cats. 709 47

The protective effect of vinpocetine on experimental brain ischemia was studied in stroke-prone spontaneously hypertensive rats (SHRSP) with bilateral carotid artery occlusion (BCAO) and in Wistar-Kyoto rats (WKY) subjected to BCAO and hemorrhage (1% of body weight). In SHRSP with BCAO, intraperitoneal (i.p.) injection of vinpocetine (1 mg/kg) 10 min before BCAO significantly prolonged the time required for the onset of ischemic seizure from 65 +/- 13 min (mean +/- SEM) to 117 +/- 19 min. In WKY with BCAO and hemorrhage, vinpocetine (5 mg/kg, i.p.) reduced the lactate level in the cerebral cortex from 11.6 +/- 2.7 mmol/g to 5.9 +/- 1.2 mmol/g and elevated the concentration of ATP from 2.05 +/- 0.09 mmol/g to 2.25 +/- 0.03 mmol/g. These results suggest a protective effect of vinpocetine against brain ischemia.
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PMID:[Protective effect of vinpocetine on experimental brain ischemia]. 715 92

We studied 18 patients (age range, 53-90 yr) with at least one cardiovascular risk factor who were treated with electroconvulsive therapy (ECT) and compared effects of five pretreatments: no drug; esmolol, 1.3 or 4.4 mg/kg; or labetalol, 0.13 or 0.44 mg/kg. Each patient received all five treatments, during a series of five ECT sessions. Pretreatment was administered as a bolus within 10 s of induction or anesthesia. Doses of methohexital and succinylcholine were constant for the series of treatments and the assignment to no drug or to drug and dose was determined by randomized block design. Measurements of systolic and diastolic blood pressure (SBP, DBP) and heart rate (HR) were recorded during the awake state and 1, 3, 5, and 10 min after the seizure. The deviation of ST segments from baseline was measured by an electrocardiogram (ECG) monitor equipped with ST-segment analysis software. The results (mean +/- SEM) show that without pretreatment, there were significant (P < 0.05) peak increases in SBP and HR (55 +/- 5 mm Hg and 37 +/- 6 bpm, respectively), recorded 1 min after the seizure. Comparable reductions (by approximately 50%) in these peak values were achieved after esmolol (1.3 mg/kg) or labetalol (0.13 mg/kg), and cardiovascular responses were nearly eliminated after the same drugs in doses of 4.4 and 0.44 mg/kg, respectively. The deviation of ST-segment values from baseline in any lead was not measurably influenced by either antihypertensive drug. SBP values were lower after labetalol 10 min after the seizure, but not after esmolol. Asystolic time after the seizure was not significantly longer with either drug.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative effects of esmolol and labetalol to attenuate hyperdynamic states after electroconvulsive therapy. 786 25


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