Substance and alcohol actions/misuse最新文献

A survey of treatment results is presented, using a variety of guidelines for the therapy of different features of heroin addiction in a toxicology unit. Data on 3,211 inpatients under treatment from 1972 are analyzed separately, as well as the follow-up status of 1,262 outpatients who were enrolled in a methadone treatment program. The results are discussed in terms of reliability of the programs and their risk-benefit ratios for the community.

A single dose of ethanol induced a bimodal increase of Fe++- and ascorbic acid-stimulated lipid peroxidation in mouse brain crude synaptosomal preparations. This effect of ethanol was lost in preparations from ethanol tolerant animals and reappeared when the animals recovered from tolerance after withdrawal from ethanol treatments. The parallel changes in lipid peroxidation of brain crude synaptosomal preparations with the development and disappearance of tolerance to ethanol imply that the effect of ethanol on brain lipid may be directly associated with its mechanism in the CNS.

Chronic ethanol treatment effects a decrease in K+-stimulated endogenous glutamate release and an increase in glutamate levels in rat frontal cortex. This treatment also increases (3H)-glutamate uptake in striatal and hippocampal slices. No uptake changes were observed in either cortical slices or synaptosomes. Ethanol withdrawal increases K+-stimulated glutamate release in cortex and hippocampus and glutamate levels in cortex, striatum and hippocampus. (3H)-glutamate uptake is increased in striatum of withdrawn animals. Thus, regional variations were observed with regard to both effect and degree of effect. Because in vitro and acute ethanol treatments had no effect on uptake or release, these changes probably result from activated feedback mechanisms that attempt to compensate for ethanol's action on brain systems rather than direct effects on membrane structure. Combined level-release data suggest an effect of ethanol on glutamate distribution in cortex and striatum. Combined uptake and release data indicate a correlation between diminished glutamate synaptic activity and the addicted state, and between heightened glutamate synaptic activity and the withdrawn state.

The literature on elderly alcohol and drug use and abuse is reviewed. Factors in old age which influence usage patterns, risks, clinical presentations, diagnosis and treatment are emphasized. Several themes for clinical research are defined. While substance abuse is less prevalent in the elderly than in younger cohorts, it is common enough to constitute a significant public health problem, may increase in the future, is often overlooked by clinicians, and may be successfully managed if treatment is tailored to the special requirements of this age group.

A number of investigators have concluded on the basis of a substantial and compelling body of biochemical, pharmacological and behavioral evidence, that opiates and particularly morphine, directly block central dopamine (DA) receptors. This evidence includes the recent finding that cataleptogenic doses of morphine suppress 3H-spiroperidol binding to striatal membranes ex vivo. On the other hand, an important albeit relatively sparse literature of experimental evidence exists suggesting that morphine and other mu-receptor opiates do not directly bind to central dopaminergic receptors. The most convincing evidence to this effect are behavioral findings that morphine potentiates rather than inhibits the stereotyped behavior induced by the direct DA agonist apomorphine and biochemical evidence demonstrating a failure of 3H-morphine or 3H-dihydromorphine to specifically bind central DA receptors in striatal tissue. (Indeed, even those reports that demonstrated a morphine induced suppression of 3H-spirioperidol labelling of DA receptors failed to find a direct effect on post-synaptic receptors.) Evidence is presented in this report to show that morphine acts presynaptically to acutely inhibit DA release, and thus, that morphine inhibition of DA receptor mediated responses is indirect, being the result of an inhibition of pre-synaptic DA release rather than a direct effect exerted on post-synaptic DA receptors themselves.

One of the presumed effects of ethanol is the suppression of acetylcholine release at presynaptic sites. If these neuronal effects are associated with CNS depression, then administration of a cholinesterase inhibitor (physostigmine) with ethanol should result in antagonism of this CNS depression. In the present study electrophysiological measures of sleep were used to assess the degree of CNS depression in response to ethanol alone (2.0 g/kg), physostigmine (1.0 mg/kg) alone, and the combination of both drugs administered together. These results were evaluated with respect to a saline control. Our findings indicate an antagonism between ethanol and physostigmine; the shortened sleep latency observed in animals receiving ethanol was reversed to control levels with administration of physostigmine.

Rabbits treated with a single IV dose of ethanol, 0.6 g/kg, exhibited rapid EEG synchronization and behavioral changes that were reversed and, in part, prevented by the opiate antagonist, naloxone, 40 micrograms/kg. The continuous intracerebroventricular infusion of acetaldehyde, 10 or 120 micrograms/min. caused biphasic changes with EEG activation and severe bradycardia followed by overt synchrony during the post-infusion period. The results of the present study provide further evidence for the ability of naloxone to counteract some acute effects of ethanol. Moreover, they do not support a role of acetaldehyde itself as mediator of EEG changes associated with mild alcohol intoxication.

The multiplicity of the interaction products of FeCl3 and KI are adequate to detect drugs bearing a nitrogen group, bases, imides, purines, in particular. To take advantage of the chemical ability of the two constituents of the reagent singularly they are applied to the plate in sequence. FeCl3 will act as a positive ion Fe+3 and it will chealate, oxidate, and produce salts. KI by reacting with FeCl3 will produce a new chemical specie, for example, Fe(Cl3I3)6(-3), Werner complexes, and production of elemental iodine that further interacts with KI and drugs facilitating detection with adequate sensitivity and for practical use.