PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Dextroamphetamine”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1978

Methylphenidate vs dextroamphetamine vs caffeine in minimal brain dysfunction: controlled comparison by placebo washout design with Bayes' analysis.

Double-blind crossover comparison of methylphenidate hydrochloride, dextroamphetamine sulfate, and caffeine after placebo washout in 29 children with minimal brain dysfunction (MBD) showed on six ratings that methylphenidate and dextroamphetamine were significantly (P less than .05 to P less than .001) better than placebo and caffeine, but not significantly (P less than .05) different from each other. Placebo, caffeine, and ratings before drug did not differ significantly. Of 26 drug responders, 12 responded best to dextroamphetamine, ten to methylphenidate, and one to caffeine. The latter child showed no improvement at all with either prescription stimulant. Methylphenidate and dextroamphetamine were each efficacious for six children who did not respond to the other stimulant. All three drugs showed significant (P less than .05) weight loss and cardiovascular side effects, the latter possibly spurious. Dextroamphetamine showed a significant (P less than .05) decrease from placebo in "tummyaches."

Attention Deficit Disorder with Hyperactivity↗
PubMed1977

Dextroamphetamine with morphine for the treatment of postoperative pain.

In a double-blind, single-dose study, dextroamphetamine combined with morphine was compared with morphine alone to determine the relative efficacy of the combination given intramuscularly for postoperative pain. Each of 450 patients received one treatment of morphine sulfate (3, 6 or 12 mg) with dextroamphetamine (0, 5 or 10 mg). Analgesia, as measured by the patients' subjective responses to questions about relief of pain, was augmented when dextroamphetamine was given with morphine; the combination of dextroamphetamine, 10 mg, with morphine was twice as potent as morphine alone, and the combination with 5 mg was 1 1/2 times as potent as morphine. In simple performance tests, and in measures of side effects, dextroamphetamine generally offset undesirable effects of morphine (sedation and loss of alertness) while increasing analgesia. Effects on blood pressure, pulse and respiratory rate were minimal.

Adult↗
PubMed1977

The effect of the stimulant drugs, dextroamphetamine and methylphenidate, on secretion of growth hormone in hyperactive children.

The stimulant effect of L-dopa (125 to 500 mg) was compared to dextroamphetamine and methylphenidate, 15, and 20 mg, respectively, on growth hormone secretion in 20 hyperactive children. All three stimulants were responsible for peak GH concentration in serum at 60 minutes after drug ingestion; there was no significant difference between the mean GH level at any time of sampling. Seven of the children were retested with L-dopa and dextroamphetamine after six to eight months of treatment with methylphenidate. After treatment, there was a tendency to higher zero time levels of GH, and to delayed and/or paradoxical response to dextroamphetamine. The findings indicate an acute and a probably long-term effect of dextroamphetamine and methylphenidate on the homeostasis of growth hormone. The possible long-term adverse effects of these drugs on the growth of children indicates the need for caution to the widespread use of these agents.

Adolescent↗
PubMed1979

The effects of LSD-25 and dextroamphetamine on the use of defensive language.

Verified that psychotomimetics attenuate verbal defense mechanisms. This was accomplished by reanalyzing the 5-minute monologues of 7 neurotic depressives who participated in a project (Mechaneck, Feldstein, Dahlberg, & Jaffe, 1968) that examined the effects of LSD and dextroamphetamine on timing aspects of speech. Dosages were subhallucinatory: 15-25 mg dextroamphetamine, 50-100 mg LSD, and a matching placebo. Volunteers received each drug (double-blind) seven or eight times on a random schedule over a 1 1/2-year period; there was a 3-week intertrial interval. The patient provided 5-minute monologues both before and after drug effects. The monologues were transcribed and scored for formal measures of defensive language. Results indicated that LSD caused individuals to make more personal statements and to use explanation and evaluations less often. Dextroamphetamine was found to decrease the use of nonpersonal references.

Adult↗
PubMedDate not supplied

Mutagenicity obtained experimentally by oral administration of dextroamphetamine sulphate to the rat.

Research work on the possible mutagenic effects of the amphetamine, sympathomimetic amine, was carried out on the rat. The method used was the dominant lethal assay, in its sub-acute form. Dextroamphetamine sulphate was administered orally. At the dosage and frequency of the test, dextroamphetamine sulphate was found to be a significantly mutogenic agent. The over-all mutagenic index was 13.92% (P less than 0.01) for the test group and 8.90% for the control group.

Abnormalities, Drug-Induced↗
PubMed1977

Subjective responses and excretion patterns of dextroamphetamine after the administration of therapeutic doses.

Twelve male medical and graduate students received dextroamphetamine sulfate in doses of 0, 5, 10, and 15 mg/70 kg body weight. The study was conducted in a double-blind manner, and treatments were assigned according to randomized, complete block design. The drug was given orally and subjects were instructed not to eat 3 1/2 h prior to administration. After administration, total urine output was collected for 12 h; no attempt was made to control urinary pH to more realistically approach the general clinical usage of amphetamines. The urine was pooled into two 6-h segments and analyzed for amphetamine concentration. Subjective impressions of the treatments were also evaluated by means of the Cornell Medical Index Questionnaire. Results showed that approximately 30% of the total dose was excreted unchanged within 12 h after administration. The amount excreted agreed very closely with the doses given and paralleled the scores for subjective impressions by the subjects. None of the subjects felt that their driving would be impaired for any of the doses administered. This study indicates that under ordinary conditions (in which pH is not artificially controlled), therapeutic doses of dextroamphetamine can be detected in urine for up to 12 h after oral administration.

Administration, Oral↗
PubMed1978

The effects of dextroamphetamine on kinesthetic figural aftereffects.

The effect of dextroamphetamine, primarily a central stimulant, on kinesthetic figural aftereffects (KFAEs) was examined. The subjects were selected after preliminary testing with the Eysenck Personality Inventory and were classified into three groups: extraverts, ambiverts, and introverts. d-Amphetamine was used at three dose levels and a control group was included for purposes of comparison. The 3 X 4 randomized block design was replicated ten times. KFAEs were measured under two sets of conditions, i.e., before and after the induction experience. The results support the following conclusions: (1) neither personality grouping nor drug treatment during preinduction trials significantly affected KFAE; (2) both types of variables were, however, significantly related to behavior during the postinduction trials; (3) the extraverted subjects showed larger KFAEs than ambiverted and introverted subjects under placebo condition; (4) the extent of KFAE was reduced in extraverted and enhanced in introverted subjects under the influence of the drug; (5) there were significant interactions between the drug treatments and personality variables in effects on KFAE.

Adolescent↗
PubMed1978

Dextroamphetamine: cognitive and behavioral effects in normal prepubertal boys.

The behavioral, cognitive, and electrophysiological effect of a single dose of dextroamphetamine (0.5 milligram per kilogram of body weight) or placebo was examined in 14 normal prepubertal boys (mean age, 10 years 11 months) in a double-blind study. When amphetamine was given, the group showed a marked decrease in motor activity and reaction time and improved performance on cognitive tests. The similarity of the response observed in normal children to that reported in children with "hyperactivity" or minimal brain dysfunction casts doubt on pathophysiological models of minimal brain dysfunction which assume that children with this syndrome have a clinically specific or "paradoxical" response to stimulants.

Attention Deficit Disorder with Hyperactivity↗
PubMed1979

Norepinephrine metabolism and clinical response to dextroamphetamine in hyperactive boys.

The 24-hour urinary catecholamine metabolites 3-methoxy-4-hydroxyphenylglycol, normetanephrine, and metanephrine were measured in 23 hyperactive boys and 13 matched healthy controls. The hyperactive children excreted lower MHPG and higher NM (low MHPG/NM ratio) amounts than in controls. The administration of d-amphetamine in the dose of 0.5 mg/kg body weight divided over two doses daily for two weeks decreased MHPG excretion in the hyperactive children. When the hyperactive children group was divided into drug responders and nonresponders according to their pre- and post-treatment scores on the Conners Teacher Questionnaire, d-amphetamine administration decreased MHPG excretion in the responders and did not change it in the nonresponders. Percent decrease in MHPG excretion correlated significantly with percent change in the hyperactivity factor of the questionnaire on the Spearman Rank Order Correlation Coefficient. Pretreatment urinary metabolites did not differentiate the responders from nonresponders. It is suggested that a relationship between CNS norepinephrine metabolism and hyperactivity exists and that d-amphetamine may achieve its therapeutic action in hyperactive children by altering CNS NE metabolism.

Central Nervous System↗
PubMed1979

Effects of dopamine agonists and antagonists in Tourette's disease.

The actions of haloperidol, dextroamphetamine sulfate, levamfetamine succinate, apomorphine, and piribedil were studied in two patients with Giles de la Tourette's disease in an attempt to clarify the catecholamine mechanisms involved in this condition. Both dextroamphetamine and levamfetamine increased the severity of the symptoms; dextroamphetamine was more potent. Haloperidol controlled the symptoms and also antagonized the effect of dextroamphetamine. Apomorphine injections reduced the severity of symptoms, even in the presence of dextroamphetamine. We conclude that dopamine rather than norepinephrine is the principal catecholamine responsible for the symptoms. The effect of apomorphine may be understood through its action on postulated presynaptic inhibitory dopamine receptors, or other presynaptic mechanisms of action.

Adolescent↗
PubMed1975

Methysergide in the treatment of narcolepsy.

Five patients with narcolepsy (four with the allied symptom of cataplexy) were treated with the serotonin antagonist methysergide. All patients had as good control of their sleep attacks while on methysergide therapy as on a control period of dextroamphetamine therapy. The cataplexy was less well controlled by methysergide than by dextroamphetamine, but improved when compared to a period without medication. Two patients developed severe calf claudication while on methysergide.

Adult↗
PubMed1978

Gamma hydroxybutyrate in the monkey. IV. Dopaminergic mechanisms.

The electrical seizure activity and trancelike state induced in the rhesus monkey by gamma-hydroxybutyrate (GHB) were abolished by dextroamphetamine. Dextroamphetamine blockade of this neurophysiologic effect was overcome with chlorpromazine, a dopamine receptor blocker. These results suggest that the electroencephalographic (EEG) and behavioral effects of GHB are related to effects on dopaminergic systems. Such a relationship, if substantiated by further studies, might indicate that anticonvulsant drugs used to treat petit mal epilepsy have a dopaminergic mode of action.

Animals↗
PubMed1979

Amphetamines reduce embryonic size and produce caudal hematomas during early chick morphogenesis.

Experiments were designed to study some of the similarities and differences in the effects of amphetamines and trypan blue on early chick morphogenesis. Both dextroamphetamine sulfate (0.5 mg/egg) and methamphetamine hydrochloride (1.0 mg/egg) were capable of inducing, in 3-day chick embryos, caudal hematomas which were similar in appearance and location to those routinely observed following treatment with trypan blue. It was found, too, that both dextroamphetamine and methamphetamine treated embryos frequently exhibited a significant decrease in crown rump length and cross-sectional area of the notochord, neural tube, dorsal aortae and whole body section, when compared with unopened or saline injected controls. Trypan blue treated embryos had only a rare decrease or increase in the size of structures when compared to either control group. These findings suggest that the amphetamines have an ability to decrease or retard embryonic growth in the chick.

Abnormalities, Drug-Induced↗
PubMed1976

Cardiomyopathy associated with amphetamine administration.

A 45-year-old woman with congestive heart failure, in whom there was no evidence of coronary heart disease, valve disease, or other demonstrable cause of heart failure, was found to have taken high doses of dextroamphetamine over a long period. Withdrawal of amphetamine resulted in deterioration, suggesting a physical cardiac dependence on the drug. The clinical and autopsy findings are presented and the similarities to the myocarditis associated with pheochromocytoma are discussed. The evidence presented suggests a causal relationship between administration of dextroamphetamine and the cardiomyopathy.

Amphetamines↗
PubMed1977

Gilles de la Tourette's syndrome. Familial occurrence and precipitation by methylphenidate therapy.

Gilles de la Tourette's syndrome was independently ascertained in two male cousins once removed. Previous studies have shown familial clustering of individuals with tics, but no consistent pattern of inheritance of Tourette's syndrome has been apparent. The onset and later exacerbation of symptoms in our younger patient were associated with the administration of CNS stimulants given for excessive motor activity. The adverse effects of methylphenidate and dextroamphetamine therapy on Tourette's syndrome supports the hypothesis that this condition results from a relative excess of CNS catecholaminergic activity. Physicians prescribing these agents should inquire about the presence of tics in patients and their families.

Adult↗