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At least 19 recordsLinked to original sources
PubMedDate not supplied

Pulmonary hypertension, "plexogenic pulmonary arteriopathy" and the appetite depressant drug aminorex: post or propter?

An epidemic of chronic pulmonary hypertension of vascular origin (CPHVO) has occurred in Austria, the Federal Republic of Germany, and Switzerland. The epidemic started in 1967 and reached its peak in 1968 and 1969. Since 1972, the prevalence of patients with CPHVO among individuals investigated by cardiac catheterization is again as low as in the pre-epidemic years. In Bern the prevalence of CPHVO during the peak of the epidemic was 20 times higher than during the 12-year period preceding the epidemic. The clinical, physical, electrocardiographic, radiologic, haemodynamic and respiratory findings of the patients observed in Bern (n = 102) are summarized. There has been a mortality between 12 and 20% at the time of the epidemic. Most patients observed for the first time during the epidemic have remained severely disabled over the years. A minute fraction seems to have recovered. There is a close geographic as well as temporal relation of the epidemic to the marketing and intake of the appetite depressing drug aminorex fumarate (Menocil). Acute administration of aminorex leads to a transient rise of the pulmonary artery pressure and vascular resistance in a number of animal species. It has not been possible to produce sustained precapillary pulmonary hypertension and chronic cor pulmonale vasculare under the conditions of chronic administration of the drug in the species tested. Morphologic examination of lung biopsy and autopsy material of patients who have died from CPHVO after the intake of aminorex reveals the presence of "plexogenic pulmonary arteriopathy". The vascular lesions are identical with those observed in pulmonary hypertension due to large congenital left-to-right shunts. In balancing the pros and cons, it appears that the arguments in favour of a cause-effect relationship between aminorex and pulmonary hypertension, which are derived from epidemiological evidence, outweigh the results of "negative" animal experiments. A "propter" in the title of this paper, therefore, seems to be more appropriate than a post".

Adolescent↗
PubMed1977

Nutritional implications of renal disease. IV. Nutritional aspects of chronic renal insufficiency in childhood.

Nutritional treatment of children with renal insufficiency presents special problems related to undernutrition, i.e., insufficient caloric intake to permit normal growth, vitamin D intake, and protein needs, as well as depressed appetite. With regard to energy, it is suggested that uremia may lead to increased caloric requirements, thus exacerbating growth depression. Protein requirements, which actually may not be as important as caloric needs, have not been determined for uremic children. Another factor in growth failure in such children involves vitamin D metabolism and its role in renal osteodystrophy. Successful dietary management of these various interrelated aspects of childhood renal disease requires sensitive, knowledgeable personnel.

Acidosis↗
PubMed1979

Changes in weight during treatment for depression.

Changes in appetite and weight were examined in a group of 47 carefully diagnosed primary depressives who were treated in a random design with either placebo (N = 17) or amitryptyline (N = 30) over a 35-day protocol. While the amitriptyline treated group as a whole showed a greater gain in weight than did the placebo group (4.5 vs. 0.5 lb, p less than 0.05), no differential effects could be demonstrated between drug responders and nonresponders. Likewise, while a consistent relationship between the self-report of decreased appetite and final weight change was noted in the placebo group, no simple relationship between final weight change and self-reported changes in appetite were apparent in the drug-treated patients. There was, however, a relationship between the report of decreased appetite and clinical severity of depression in the drug nonresponder subgroup despite significant weight gain during the protocol. Thus, weight change during this study period did not appear to show a simple relationship to corresponding clinical change. The clinical lore that has supported the notion that increased appetite and weight gain in patients being treated with tricyclic antidepressants are "good" signs cannot be confirmed by our findings.

Adult↗
PubMed1978

3-Aryl- and 3-hydroxy-3-aryloctahydropyrido[2,1-c][1,4]oxazines. Synthesis, stereochemistry, and central nervous system pharmacological actions.

A series of substituted 3-aryl- and hydroxy-3-aryloctahydropyrido[2,1-c][1,4]oxazines has been synthesized for purposes of investigating potentially useful CNS pharmacological actions of this novel heterocyclic system. The preferred conformation of the bicyclic system of the parent compounds, 1 and 2, has been shown to be trans with equatorial orientation of the 3-phenyl substituent in each compound. The various substituted aryl analogues of this series are depressants of motor activity in mice, and certain analogues exhibit significant anticonvulsant and appetite suppressant activity in test animals.

Animals↗
PubMed1977

Anorexic and behavioural effects of a new imidazo-isoindole derivative (mazindol) in comparison with d-amphetamine in the rat.

The effect of an imidazo-isoindole derivative (mazindol) upon motor and feeding activity and two different avoidance behaviours have been compared with those of d-amphetamine in rats. It was found that both drugs depress feeding activity in a dose-related manner and increase the motor activity of the animals. However, the ratio of the lowest motility-increasing dose and the lowest appetite suppressant dose is 0.5 for d-amphetamine and 2 for mazindol. Mazindol, like d-amphetamine, caused a stereotyped behaviour in rats when given in very high doses, but the range between the anorexic and the stereotyped behaviour dose is much higher for mazindol than for d-amphetamine. The shuttle-box avoidance behaviour suppressed by tetrabenazine is completely restored by d-amphetamine and partially by mazindol. Lever-pressing avoidance suppressed by tetrabenazine is restored by d-amphetamine while mazindol at the doses used is ineffective. It is concluded that mazindol could be an anorexic agent better suited than d-amphetamine for clinical use.

Animals↗
PubMed1979

Effect of cocaine on food intake in rats.

In rats trained to eat during a five-hour daily period, cocaine (10, 15, and 25 mg/kg) depressed food intake. The anorexia was seen during the 1st h only, with no effect on total food intake.

Animals↗
PubMed1977

Metabolic regulation as a control for lipid disorders. I. Influence of (--)-hydroxycitrate on experimentally induced obesity in the rodent.

The feasibility of treating obesity by metabolic regulation has been explored in this study by examining the effect of (--)-hydroxycitrate on three types of experimentally induced obesity in the rodent.(--)-Hydroxycitrate was utilized because it depressed fatty acid and cholesterol synthesis in vivo through its activity as a potent competitive inhibitor of APT citrate lyase. In all models, the mature rat, the goldthioglucose-induced obese mouse, and the ventromedial hypothalmic lesioned obese rat, food intake and body weight gain were reduced signficantly by the chronic oral administration of a nontoxic dose of (--)-hydroxcitrate. Body composition analyses of mature rats treated with (--)-hydroxycitrate demonstrated a significant depression of body lipid levels and an unaltered body protein content. However, a citrate administration produced no significant effects on weight gain, food intake, or body lipid or protein levels when compared to controls.

Animals↗
PubMed1978

Drugs and depression.

Moderate or severe depression is now one of the most common diseases of our time with a prevalence of nearly 3%. It seems likely that this prevalence has increased as a result of the wider use of drugs which have an effect on the neurotransmitters. Changes in the levels of these neurotransmitters in the central nervous system are thought to be the biochemical basis for the development of at least some depressive illnesses. Drug-induced depressions are more likely to occur in those individuals who are genetically predisposed to depression or who have had a previous depressive illness. Other groups who are particularly susceptible to these effects are the elderly. Many groups of drugs have a primary or secondary action on the central nervous system neurotransmitter function. Some 200 drugs have been claimed to cause depression in certain patients, but only a relatively small number precipitate depressive symptoms with any frequency. Those most commonly implicated are the long-acting antipsychotics, barbiturates, ethanol, oral contraceptives and antihypertensive agents. It is important to remember that some drugs, such as reserpine, cause depression as a side-effect during their therapeutic use whereas others, such as fenfluramine, cause depression mainly when they are withdrawn too rapidly. In those patients presenting with depression, it is important to review the current drug therapy in order to assess the part played by these drugs in the development of the depression. Following this assessment, drug therapy should be adjusted appropriately. However, a distinction must be made between the symptoms of depression, those physiological changes which occur during treatment with a variety of drugs, and the patient's reaction to the disease for which they are being treated.

Analgesics↗
PubMed1977

Effect of toloxatone on behaviour of primates.

1. The effects of (3-methyl)-3-phenyl-5-hydroxy-methyl-2-oxazolidinone (toloxatone) were studied on the behaviour of three species of primates: baboon, rhesus monkeys and chimpanzee. 2. The activity against reserpine-induced depression is observed in baboon as in rodents. 2. The administration of toloxatone induces three effects which probably have the same origin: suppression of feeding inhibition of the subordinate baboon, improvement of escape reaction in the conditioned chimpanzee, increase in general activity and the active component of social behaviour in grouped rhesus monkeys. These three effects can be interpreted as resulting from the stimulating effect of toloxatone, or more precisely from a disinhibiting effect. 4. Contrary to amphetamine, toloxatone does not induce, even at high or repeated doses, behavioural disturbances.

Administration, Oral↗
PubMed1979

Effect of anorexic drugs on food intake and the micro-structure of eating in human subjects.

Human volunteer subjects of normal weight received oral doses of (+)amphetamine (10 mg) or (+/-)fenfluramine (30 mg and 60 mg) together with a placebo control according to a within-subjects design. The effects of these treatments were monitored by measuring food intake in a test meal, subjective ratings of hunger motivation and the micro-structure of eating behaviour abstracted from videotaped recordings of the test meal. Various measures of the rate of feeding were computed from these recordings. Amphetamine and fenfluramine (60 mg) showed generally similar effects on food intake and on the subjective experience of hunger, but displayed differing actions on the fine structure of eating. Amphetamine increased latency to initiation of eating and increased the rate of food ingestion, whilst fenfluramine slowed the local rate of eating and eliminated the characteristic decline in the rate of feeding across the course of a meal. These findings display certain resemblance to the results of animal experiments involving similar pharmacological manipulations and emphasise the importance of measuring rate of feeding in animal and human studies. The results of this study suggest that the micro-analysis of feeding behaviour not only provides a tool for understanding systems involved in the modulation of food consumption but also reveals information which may be helpful for the use of drugs in the treatment of obesity.

Adult↗
PubMed1979

The effect of propranolol phentolamine and pimozide on drug-induced anorexia in the mouse.

Pimozide was a potent antagonist of (+)amphetamine, diethylpropion, mazindol and phentermine anorexia in the mouse. Phentolamine and propranolol produced no such antagonism, but either potentiated or had no effect on the drug-induced anorexia. Although the mechanism of action of the four anorectic agents appears to involve dopamine receptor agonist activity, an antagonist or partial agonist effect at noradrenergic receptors may also be involved.

Animals↗
PubMed1977

Anorexigenic and ancillary actions of MK-212 (6-chloro-2-(1-piperazinyl)-pyrazine; CPP).

In rats allowed to eat for 2 h/day and injected i.p. 30 min before feeding, MK-212, ED50 = 1.5 mg/kg, was two times more potent as an anorexigen than fenfluramine. However, the compounds were equiactive in the rat following p.o. administration 1.5 or 3 h before the test, while fenfluramine was more potent if the interval was extended to 6 h. In cats permitted to eat for 3 h/day, the ED50 dose (mg/kg p.o.) for MK-212 determined at 0.5, 1 and 3 h after feeding was, respectively, 15, 10, and 3 times less than that of fenfluramine. Emesis and diarrhea were frequently observed ancillary effects in cats treated with fenfluramine, whereas apparent sedation and salivation were commonly detected in animals after MK-212. In rats or cats pretreated with methergoline, the decrease in food consumption elicited by MK-212 was markedly inhibited, suggesting that the mechanism of action involves a serotoninlike effect. Compared with the marked stimulant action of amphetamine, MK-212 had only a minor and inconsistent effect on motor activity in rats and mice. Similar results were obtained with fenfluramine. MK-212 was not self-administered by rats, while the self-administration of amphetamine and morphine were demonstrated using the same experimental protocol.

Animals↗
PubMed1979

Chlorophenylpiperazine: a central serotonin agonist causing powerful anorexia in rats.

Meta-chlorophenylpiperazine inhibited serotonin and noradrenaline uptake by synaptosomes to the same extent with IC50 of 1.3 x 10(-6) M and 5.8 x 10(-6) M respectively. Dopamine uptake was less affected by meta-chlorophenylpiperazine (IC50 of 2.2 x 10(-5) M). Unlike d-amphetamine and d-fenfluramine, the drug did not significantly increase monoamine release in synaptosomal preparations. On the other hand, metachlorophenylpiperazine showed an IC50 of 620 nM in displacing 3H-5HT binding to brain membranes. Meta-chlorophenylpiperazine produced a dose-dependent reduction of food intake and this effect was prevented by a pretreatment with methergoline, a serotonin antagonist. The effect of metachlorophenylpiperazine was not modified by an intraventricular injection of 6-hydroxydopamine, electrolytic lesions of nucleus medianus raphe or ventral noradrenergic bundle, nor by a pretreatment with penfluridol, propranolol or phentolamine. The data suggest that the decrease of food intake induced by metachlorophenylpiperazine depends on its ability to act as a serotonin agonist is the brain. The specificity of the effects on serotonin suggests that this compound could prove an important tool for studies aimed at elucidating the functional role of serotonin in the central nervous system.

Animals↗
PubMed1978

A comparison of the food intake suppression produced by giving amphetamine as an aversion treatment versus as an anorexic treatment.

Separate groups of rats were given either 1 or 2 mg/kg injections of amphetamine 30 min before or after eating a preferred high-fat food. When given before eating as an anorexic treatment, amphetamine initially suppressed intake almost completely, but with repeated injections tolerance developed. In contrast amphetamine given after eating as an aversion treatment initially had little effect on intake, but with repeated injections it suppressed intake almost completely in rats receiving the higher dose.

Amphetamine↗
PubMedDate not supplied

Long term effects of the anorectic agent fenfluramine alone and in combination with aminorex on pulmonary and systemic circulation in the pig.

We have investigated the effects of chronic oral administration of two anorectic substances, fenfluramine and aminorex, especially on the pulmonary circulation in young pigs with one ligated pulmonary artery. The pulmonary vascular reactivity was tested by alveolar hypoxia, alveolar hyperoxia and infusion of prostaglandin F2ALPHA. No elevation of pulmonary arterial pressures or resistances were found due to the intake of fenfluramine or aminorex over a three month period. The responses to the vasoconstrictor stimuli, hypoxia and prostaglandin F2alpha, and to the vasodilator stimulus, hyperoxia, were equal and not augmented in the drug groups. Fenfluramine or aminorex could therefore could therefore not be shown to have an adverse effect on the pulmonary circulation or on the reactivity of the pulmonary vascular bed in the pig, but fenfluramine elevated systemic arterial pressure.

Aminorex↗
PubMed1977

A pharmacologic comparison of 3,4-methylenedioxyamphetamine and LSD in the chronic spinal dog.

MDA (2.0 and 2.2 mg/kg) was compared to LSD (10 microgram/kg) and d-amphetamine (3.2 mg/kg) in single dose, antagonism, cross tolerance and appetite suppression studies. In single doses MDA specifically resembled d-amphetamine by producing marked mydriasis, nictitating membrane retraction, stereotypy and darting eye movements and LSD by markedly facilitating the flex or reflex, producing continuous stepping, whining and eye tracking movements. LSD and MDA increased respiration, body temperature and the latency of the skin twitch reflex and produced behavioral arousal. Cyproheptadine antagonized the effects of LSD but was ineffective against MDA. Phenoxybenzamine antagonized the respiratory, pupillary and hyperthermic effects of MDA and the respiratory effect of LSD. Chlorpromazine antagonized many of the effects of LSD and MDA. Spinal dogs were made tolerant to the behavioral and physiologic effects of LSD. Cross tolerance developed to some but not all of the effects of MDA. In intact dogs MDA was 1/10 as potent as d-amphetamine in suppressing appetite. It is concluded that MDA has properties resembling both LSD and amphetamine.

3,4-Methylenedioxyamphetamine↗