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At least 1,081 records · Page 60Linked to original sources
PubMed1985

Studies on brain monoamine neurotransmitters in mice after prenatal exposure to barbiturate.

Pregnant HS/Ibg mice received 3 g/kg phenobarbital in their milled food; control dams received unadulterated milled food. Their offspring were tested on ages 22 and 50 days for norepinephrine (NE) and dopamine (DA) levels and DA turnover in the hypothalamus and striatum. Additional groups were tested on days 8, 22, and 50 for brain stem tryptophan hydroxylase (TPH) activity. Hypothalamic DA level among offspring with prenatal PhB exposure (B offspring) was 37% below control level on age 22 days and 61% below control on day 50 (p less than 0.001). Hypothalamic NE level of B offspring was reduced on age 50 days (52%, p less than 0.05) and not on day 22. DOPAC level and DA turnover did not differ among B and control groups. Prenatal exposure to PhB did not have a significant effect on TPH activity. The changes in catecholamines may mediate, at least in part, some of the early barbiturate induced neuromorphological and behavioral changes previously found in our laboratory.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

[Effect of isoprenaline, in mice anesthetized with pentobarbital, on the cerebral concentration of barbiturates and on the blood levels of free fatty acids].

In mice isoprenaline increases duration of pentobarbital narcosis without modification of cerebral levels. A correlation between duration of sleep and FFA seric levels increased by isoprenaline is demonstrated. This dual effect is suppressed by pindolol. These facts suggest that hepatic metabolism of pentobarbital is slowed by lipo-mobilisation.

Animals↗
PubMed2001

Spectrophotometric kinetic and determination of quinones and barbiturates.

The kinetics of 1,3-dimethylbarbituric acid with some quinones, namely 1,4-benzoquinone, 1,4-naphthoquinone and p-chloranil in 50% methyl alcohol-water mixture have been investigated spectrophotometrically at 30-50 degrees C. The reaction follows overall second-order kinetics, first order each in reactant. From the dependence of the rate constants on temperature, activation parameters have been calculated. A plot of deltaH# versus deltaS# for the reaction gave a good straight line with an isokinetic temperature of 387.66 K. The rate of reaction increases with increasing dielectric constant of the medium. Based on this reaction, a spectrophotometric determination method of quinones is described. Beer's law was obeyed within the concentration range 2.7-61.5 microg ml(-1) quinone. The method was applied for determination of barbituric, thiobarbituric and 1,3-dimethylbarbituric acids with 1,4-naphthoquinone within a concentration range of 3.2-39.5 microg ml(-1) barbiturate. The reaction mechanism and reactivity have been discussed.

Barbiturates↗
PubMed1977

The change of erythrocyte shape following action of different substances altering mg++-dependent ATPase activity (actomyosin-like protein).

It was found that some substances as aspartate, glutamate, atropine, physostigmine, ephedrine, caffeine and theophylline tended to alter the erythrocyte shape in the same concentration in which also the Mg++-dependent ATPase activity had been changed. The employment of various concentrations of barbiturate revealed that changes of the erythrocyte shape were dependent on its concentration. In the present study the relationship between Mg++-dependent ATPase and biconcave erythrocyte shape is discussed.

Adenosine Triphosphatases↗
PubMed2001

The new generation of GABA enhancers. Potential in the treatment of epilepsy.

gamma-Aminobutyric acid (GABA) is considered to be the major inhibitory neurotransmitter in the brain and loss of GABA inhibition has been clearly implicated in epileptogenesis. GABA interacts with 3 types of receptor: GABAA, GABAB and GABAC. The GABAA receptor has provided an excellent target for the development of drugs with an anticonvulsant action. Some clinically useful anticonvulsants, such as the benzodiazepines and barbiturates and possibly valproic acid (sodium valproate), act at this receptor. In recent years 4 new anticonvulsants, namely vigabatrin, tiagabine, gabapentin and topiramate, with a mechanism of action considered to be primarily via an effect on GABA, have been licensed. Vigabatrin elevates brain GABA levels by inhibiting the enzyme GABA transaminase which is responsible for intracellular GABA catabolism. In contrast, tiagabine elevates synaptic GABA levels by inhibiting the GABA uptake transporter, GAT1, and preventing the uptake of GABA into neurons and glia. Gabapentin, a cyclic analogue of GABA, acts by enhancing GABA synthesis and also by decreasing neuronal calcium influx via a specific subunit of voltage-dependent calcium channels. Topiramate acts, in part, via an action on a novel site of the GABAA receptor. Although these drugs are useful in some patients, overall, they have proven to be disappointing as they have had little impact on the prognosis of patients with intractable epilepsy. Despite this, additional GABA enhancing anticonvulsants are presently under development. Ganaxolone, retigabine and pregabalin may prove to have a more advantageous therapeutic profile than the presently licensed GABA enhancing drugs. This anticipation is based on 2 characteristics. First, they act by hitherto unique mechanisms of action in enhancing GABA-induced neuronal inhibition. Secondly, they act on additional antiepileptogenic mechanisms. Finally, CGP 36742, a GABAB receptor antagonist, may prove to be particularly useful in the management of primary generalised absence seizures. The exact impact of these new GABA-enhancing drugs in the treatment of epilepsy will have to await their licensing and a period of postmarketing surveillance. As to clarification of their role in the management of epilepsy, this will have to await further clinical trials, particularly direct comparative trials with other anticonvulsants.

Animals↗
PubMed1980

Determination of valproic acid kinetics in patients during maintenance therapy using a tetradeuterated form of the drug.

A method has been developed for measuring concentrations of valproic acid and, with stable isotopes, labelled forms of VPA, in the plasma of patients undergoing maintenance therapy. One tetradeutero isomer of valproic acid-di-(2,3-dideuteropropyl) acetic acid-has been synthesized for administration to patients. A [2H14]valproic acid-diheptadeuteropropyl acetic acid-was synthesized as the internal standard. After isolation from body fluids the acids were methylated with diazomethane. The McLafferty fragments of the methyl esters were used for mass spectrometric quantification. It was demonstrated that the [2H4]valproic acid used behaves kinetically like the unlabelled drug in the human body. One dose of [2H4]valproic acid was given as a pulse dose to epileptic patients and the elimination profile was measured during continuous normal treatment. The half-life of valproic acid in patients under barbiturate or carbamazepine co-medication was reduced to at least half the value found after single dose administration to healthy volunteers.

Epilepsy↗
PubMed1999

Blockade of glutamate receptors and barbiturate anesthesia: increased sensitivity to pentobarbital-induced anesthesia despite reduced inhibition of AMPA receptors in GluR2 null mutant mice.

BACKGROUND: Barbiturates enhance gamma-aminobutyric acid type A (GABA(A)) receptor function and also inhibit the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) subtype of glutamate receptor. The relative contribution of these actions to the behavioral properties of barbiturates is not certain. Because AMPA receptor complexes that lack the GluR2 subunit are relatively insensitive to pentobarbital inhibition, GluR2 null mutant mice provide a novel tool to investigate the importance of AMPA receptor inhibition to the anesthetic effects of barbiturates. METHODS: GluR2 null allele (-/-), heterozygous (+/-), and wild-type (+/+) mice were injected with pentobarbital (30 and 35 mg/kg intraperitoneally). Sensitivity to anesthetics was assessed by measuring the latency to loss of righting reflex, sleep time, and the loss of corneal, pineal, and toe-pinch withdrawal reflexes. In addition, patch-clamp recordings of acutely dissociated CA1 hippocampal pyramidal neurons from (-/-) and (+/+) mice were undertaken to investigate the effects of barbiturates on kainate-activated AMPA receptors and GABA-activated GABA(A) receptors. RESULTS: Behavioral tests indicate that sensitivity to pentobarbital was increased in (-/-) mice. In contrast, AMPA receptors from (-/-) neurons were less sensitive to inhibition by pentobarbital (concentrations that produced 50% of the maximal inhibition [IC50], 301 vs. 51 microM), thiopental (IC50, 153 vs. 34 microM), and phenobarbital (IC50, 930 vs. 205 microM) compared with wild-type controls, respectively. In addition, the potency of kainate was greater in (-/-) neurons, whereas no differences were observed for the potentiation of GABA(A) receptors by pentobarbital. CONCLUSIONS: The GluR2 null mutant mice were more sensitive to pentobarbital anesthesia despite a reduced sensitivity of GluR2-deficient AMPA receptors to barbiturate blockade. Our results indicate that the inhibition of AMPA receptors does not correlate with the anesthetic effects of barbiturates in this animal model. We postulate that the increase in the sensitivity to anesthetics results from a global suppression of excitatory neurotransmission in GluR2-deficient mice.

Alleles↗