Needle sharing and other behaviours related to HIV spread among intravenous drug users.
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Biomedical subjects
Publications and source records attributed to E Tempesta.
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The effects of chronic addiction to, and withdrawal from, opiates on sleep have been described in experimental animals, in human adults and infants born to addicted mothers. These sleep alterations are seen through the first weeks of life. Thirteen maternally addicted babies were studied. Sleep samples were recorded and scored within a few days following birth and repeated 4 or 5 weeks later after recovery from the abstinence syndrome. A significant decrease in quiet sleep and increase of active sleep were found. The same alterations, although less marked, were observed in a follow up recording performed during the second month of life. Sleep alterations in addicted newborns could be related to central nervous system (CNS) distress caused by withdrawal. The authors however propose a perturbation of endogenous opiates subsequent to fetal addiction as a cause of sleep alterations.
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An open, cross-over study was performed on a population of 24 geriatric patients hospitalized because of depressive syndrome. They were subdivided, according to Hamilton's Scale as modified for the aged, into low- and high-score subgroups. The study period covered 2 months. Half the patients received acetylcarnitine for 1 month and placebo thereafter (Group A); the other half received placebo and acetyl-carnitine thereafter (Group B). Statistical evaluation was twofold: parametrical analysis of variance was carried out on 4 subgroups (A1, A2, B1 and B2) and analysis of the score percentage modifications before and after treatment was performed on Groups A and B. The experimental results showed that acetylcarnitine treatment was highly effective and statistically significant in subgroups A1/B1, A2/B2, A1, B1 and B2. In particular, it should be noted that depressive tendencies were significantly modified in most groups, whereas general somatic symptoms as well as anxiety, asthenia and sleep disturbances proved to be little affected. Clinical evaluation, carried out by calculation of modifications in pre- and post-treatment score percentages, provided clear evidence that acetylcarnitine was particularly effective in patients showing more serious clinical symptoms. The drug caused no side-effects at the doses and regimens used.
Female rats were given different doses of methadone for the whole duration of pregnancy. The effects of methadone on birthweight and abstinence syndrome were studied from birth to maturation. Visual Evoked Potentials (VEP) from onset to 90 days of age were studied with averaging and frequency analysis techniques. The intensity of the withdrawal syndrome was dependent on the doses of the drug administered to the mothers, but not on the postnatal therapy (phenobarbital or methadone) administered to offspring. VEP latencies and amplitudes were not affected by fetal addiction to methadone. Thus, any long lasting alteration of spontaneous and evoked electrical activities in the visual system of fetal addicted young rats can be excluded. Only transient slight alterations of visual evoked responses are observed during the abstinence syndrome.
In this microiontophoretic study delta 2,1,2,4-triazolin-5-one [1,3-(4-m-chlorophenyl-1-piperazinyl) propyl]-3,4-diethyl hydrochloride (etoperidone, ET, Staff) was applied on rat brainstem (medullary-pontine) reticular neurones to verify its effects on the spontaneous firing and neuronal responses to administrations of 5-hydroxytryptamine (5HT), noradrenaline (norepinephrine, NA), acetylcholine (ACh) and gamma-aminobutyric acid (GABA). ET was able to depress the spontaneous firing by a dose-dependent (for a current intensity range of 40-70 nA) local anaesthetic-like mechanism. At 75 nA a reduction in the amplitude of the action potentials occurred, partially due to a non-specific effect of ET. Repeated administrations of ET caused a progressive neuronal desensitization to the inhibition (tachyphylaxis). All the excitatory neuronal responses to ACh, 5HT and NA (interpreted respectively as nicotinic cholinergic, alpha-noradrenergic, 5HT3-serotonergic) were blocked by ET, while the inhibitory responses to 5HT, NA and GABA were not affected. The analysis of the results leads to postulate for ET a postsynaptic mechanism of action.
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Acetylcarnitine is an endogenous substance, active in the CNS, but its exact role in neurotransmission is still unknown. The present study was made to analyze by means of iontophoretic administration on single neurones of the medullary-pontine reticular formation in the rat the effects of the D- and L-acetylcarnitine on spontaneous and glutamate-evoked firing and on responses to applications of some other putative transmitters, such as acetylcholine, 5-hydroxytryptamine (5-HT), gamma-aminobutyric acid (GABA) and noradrenaline. L-Acetylcarnitine increased both spontaneous and evoked discharges, and potentiated cholinergic and serotonergic responses. The D-isomer was found to be almost ineffective. Neuronal responses to L-acetylcarnitine were reduced by dihydro-beta-erythroidine and enhanced by eserine, while atropine was ineffective. L-Acetylcarnitine increased both excitatory and inhibitory responses to 5-HT and its effect on the increase in firing rate induced by serotonergic drugs was reduced by dihydro-beta-erythroidine, but not by atropine. L- and D-Acetylcarnitine did not affect GABAergic or noradrenergic transmission. These results suggest a stereospecific facilitatory action of acetylcarnitine on neuronal responses to acetylcholine and 5-HT. It is hypothesized that this action could be exerted at a presynaptic level, at least with regard to serotonergic-induced responses, and that nicotinic receptors may be involved in the synaptic mechanism of release or reuptake of both acetylcholine and 5-HT.
Preincubation of rabbit platelet-rich plasma with cocaine hydrochloride, at low and high concentrations, increased the platelet responsiveness to arachidonic acid, in terms of the aggregating response and the thromboxane production. The thromboxane levels released by collagen-stimulated platelets were increased after incubation with low concentrations of cocaine, while marked decreases were observed after incubation with high doses of cocaine. No effects on platelet aggregation induced by collagen and ADP were observed when low concentrations of cocaine were added; on the other hand, high doses of the anaesthetic were found to block the aggregating effects of these two agents. Specific studies showed cocaine to have an inhibitory activity on prostacyclin release when the aortic tissue was mechanically and thermically stimulated. By contrast, the prostacyclin synthesis by 'exhausted' aortic rings incubated with arachidonic acid appeared to be enhanced after addition of cocaine. These results lead us to believe that cocaine modifies both the Ca++ membrane binding and the extent of Ca++ influx, thereby increasing the permeability to arachidonic acid and altering the affinity of the membrane binding sites for the aggregating agents.
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Liver function tests, hepatitis B virus (HBV) markers and cell-mediated immunity were evaluated in 100 drug addicts and in 54 healthy controls. Liver damage prevalence was much higher in the drug group, both in HBV marker-positive and in marker-negative subjects. Moreover HBV marker distribution was different among addicts in comparison with controls, in which the patterns of infection overcoming were more frequent. Cell-mediated immunity assessment showed a deep depression in the addict group. These data suggest that liver damage in addicts may be due mainly to the immunologic defect, which would have a negative influence on the action of HBV and of other viral and non-viral agents.
In this microiontophoretical study trazodone (TR) was applied on rat brainstem neurones to verify its effects on spontaneous firing and neuronal responses to administrations of 5-hydroxytryptamine (5HT), noradrenaline (norepinephrine, NA) and acetylcholine (Ach). TR was able to modify the spontaneous firing likely by an indirect action, potentiated the excitatory responses to 5HT and reduced the inhibitory ones, was ineffective on the inhibitory responses to NA, while tended to antagonize the excitatory ones. Moreover TR did not show anticholinergic properties.
The main cardiovascular problems caused by heroin addiction are examined, with particular emphasis on acute pulmonary oedema, the most dangerous and dramatic complication, of which the pathogenetic, clinical, diagnostic and therapeutic aspects are described.
Irregular menstrual cycles are fairly common in drug-addicted patients. The purpose of this research is to stablish the connection between the administration of a narcotic and the onset of amenorrhoea. After a review of the literature and aetiopathogenetic hypotheses regarding ovulatory block, 39 heroin- or morphine-addicted patients personally observed during pregnancy are studied. Even relatively low doses of narcotics can impair normal ovarian function and ovulation so there is a risk that menstrual irregularities can arise even when doses are reduced.
In this pharmacological study the authors give an extensive review of existing literature regarding the activity of carnitine and acetyl carnitine on the central nervous system. Carnitine and acetyl carnitine enter the neuro-biochemical patterns in the endoneuronal system, and affect neurotransmission in synapsis.
D-L, Acetylcarnitine was applied microiontophoretically to neurones in the brainstem of the rat, to evaluate its possible effects. The results support the hypothesis that D-L, acetylcarnitine acts on the neuronal membrane, producing selective excitatory responses of the neurones examined. The possible role of this substance at the single neurone level is discussed in relation to the results obtained by investigating the interaction between D-L, acetylcarnitine and neurotransmitters, such as acetylcholine, gamma-aminobutyric acid (GABA), serotonin and noradrenaline.
Traditional medicine represents a cultural rediscovery of local traditions. The actual and potential resources in traditional medicine and the problems of integration of modern and traditional medicine are summarized. A clinical-pharmacological methodology should be applied to evaluations of the efficacy of plants and their preparations in order to delimit the toxicological aspects. Integration between traditional and modern medicine could be obtained with the collaboration of African scientists and the formation of physicians with a good knowledge of traditional medicine.