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At least 19 recordsLinked to original sources

PubMed1976

Effect of cyproheptadine and combinations of cyproheptadine and amphetamine on intermittently reinforced lever-pressing in rats.

Effects of the tryptamine antagonist, cyproheptadine, as well as of amphetamine, chlordiazepoxide, and combinations of cyproheptadine with amphetamine on lever-pressing behavior of rats were determined. A multiple, fixed-interval, 2 min fixed-ratio, 15 response schedule of water presentation was used. The three drugs affected fixed-interval fixed-ratio responding in a rate-dependent way, lower rates being more increased whereas higher rates were relatively more decreased. Cyproheptadine increased low response rates to a lesser extent than amphetamine, but increased high response rates that were little affected or only decreased by amphetamine. The combination of cyproheptadine and amphetamine increased response rates to a higher extent than either of the drugs alone. In addition, the rate-suppressant effects of the highest doses of amphetamine were also enhanced by cyproheptadine. These results show that cyproheptadine can increase nonpunished responding and suggest that cyproheptadine and amphetamine act synergistically, but through different mechanisms, upon multiple fixed-interval fixed-ratio performance.

Amphetamine↗

PubMed1979

Paradoxical short-term effects of cyproheptadine on insulin and glucagon release in the rat.

The administration of cyproheptadine (25 mg/kg; i.p.) resulted in an increase of plasma insulin and glucagon (measured using 30 K antibody) 30, 60 and 120 min after injection to fasted rats. This dose of cyproheptadine also induced a hyperglycemia whereas a lower dose (5 mg/kg; i.p.), which did not alter plasma hormone levels, was associated with a hypoglycemia. Fed rats showed a reduction of plasma insulin with a similar elevation of blood glucose after cyproheptadine. Administration of an exogenous load of arginine resulted in increases of plasma insulin and glucagon of a greater magnitude than induced by cyproheptadine, however, cyproheptadine pretreatment (25 mg/kg) completely suppressed the pancreatic response to the amino acid, resulting in blood hormone levels similar to values seen after cyproheptadine administered alone. Cyproheptadine pretreatment also prevented the hyperinsulinemia and hypoglucagonemia resulting from glucose loading. alpha-Adrenergic receptor blockade (with phentolamine), beta adrenergic receptor blockade (with propranolol) and adrenodemedullation did not alter pancreatic responsiveness to the drug.

Adrenal Medulla↗

PubMed1976

Suppression by cyproheptadine of human growth hormone and cortisol secretion during sleep.

The effect of cyproheptadine on plasma growth hormone and cortisol levels was studied in seven male volunteers with polygraphic sleep monitoring. Sleep-related growth hormone release was completely inhibited in three of the seven normal subjects by the intravenous infusion of cyproheptadine (5 mg) which was started at the onset of sleep. In the other four, growth hormone release during sleep was significantly decreased or delayed by cyproheptadine when the drug infusion was started at 7:00 p.m., 1-2 h before the onset of sleep. The usual increase in plasma cortisol in the early morning was completely suppressed in all five subjects given cyproheptadine infusions from 4:00 to 7:00 a.m. The intravenous infusion of cyproheptadine increased slow wave sleep, although the time from sleep onset to the first occurrence of slow wave sleep was not affected. In contrast, rapid eye movement sleep was significantly decreased by cyproheptadine. These results suggest that cyproheptadine inhibits growth hormone and ACTH secretion during sleep in man, possibly by antagonizing serotoninergic mechanisms although other actions of the drug are not ruled out.

Adrenocorticotropic Hormone↗

PubMed1976

On the anticataleptic action of cyproheptadine.

The anticataleptic action of cyproheptadine, a tricyclic compound known as antiserotonin, anticholinergic and antihistaminic drug in comparison to that of atropine, promethazine, imipramine, desipramine, chlorimipramine and nomifensine was studied in rats. The catalepsy induced by spiperon, pimozide or fluphenazine was antagonized by cyproheptadine, atropine and promethazine. Imipramine and nomifensine were less active, desipramine and chlorimipramine without effect. The reserpine- and alpha-methyltyrosine-catalepsy was counteracted by cyproheptadine, promethazine and nomifensine, but not by atropine or tricyclic antidepressants. Only cyproheptadine and promethazine antagonized the catalepsy caused by a combined treatment with reserpine and alpha-methyltyrosine. The pilocarpine-catalepsy was abolished by atropine, promethazine and nomifensine and unaffected by tricyclic antidepressants. Atropine and promethazine antagonized also the physostigmine-catalepsy. The catalepsy induced by both cholinomimetic drugs was not changed or increased by cyproheptadine. The results presented indicate that cyproheptadine differs in its anticataleptic activity from all the drugs used for comparison. Possible mechansims of this activity are discussed.

Animals↗

PubMed1976

Inhibition of insulin and glucagon release from the perfused rat pancreas by cyproheptadine (Periactinol, Nuran).

The tricyclic compound cyproheptadine (Periactinol, Nuran) inhibited glucose-induced insulin release from the perfused rat pancreas. Tolbutamide-stimulated insulin release was significantly reduced in the presence and completely suppressed in the absence of a substimulatory glucose concentration (5 mM). Arginine produced a slow rise of insulin release, which was completely abolished by cyproheptadine. Furthermore the biphasic glucagon release due to the stimulus was inhibited. Oxidation of 14C-glucose in isolated islets was unaltered in the presence of cyproheptadine, and pyruvate added to the perfusion medium failed to reverse the inhibitory effect on glucose induced insulin release, indicating that impaired glucose metabolism is not responsible for the inhibition. In addition, the inhibition remained unchanged when phentolamine was present, suggesting that the effect is not mediated by inhibitory adrenergic alpha receptors. Theophylline, in contrast, partly overcame the inhibition. When the calcium concentration of the medium was enhanced, the inhibitory effect of cyproheptadine was still visible, although the relative inhibition had become smaller. The results suggest that cyproheptadine blocks insulin release by affecting a fundamental step of the stimulus-secretion coupling common to peptide hormones. A participation of a calcium-antagonizing effect in the inhibition is discussed.

Animals↗

PubMed1979

The local anesthetic effect of cyproheptadine on mammalian nerve fibres.

The local anesthetic effect of cyproheptadine on nerve fibres in the rabbit's cervical vagus and sciatic nerve was studied by the single sucrose-gap technique. Local anesthetics such as procaine and tetracaine, and an antihistaminic with local anesthetic activity, diphenhydramine, were studied for comparison. Increasing concentrations of cypropheptadine, starting from 5 x 10(-5) M, produced a dose-related fall in the amplitude of the compound action potential of the vagus nerve without significant change in the resting membrane potential. A complete reversibility of the local anesthetic effect was difficult or impossible to obtain when doses greater than 1 x 10(-4) M were used. Cyproheptadine was more potent than procaine and diphenhydramine, and less potent than tetracaine in producing nerve conduction block. Frequency-dependent block was observed with cyproheptadine and the other agents at frequencies that can be considered low (1--5 Hz). Myelinated fibres of the sciatic nerves were also blocked by cyproheptadine within the same range of concentrations (1 x 10(-4) to 1 x 10(-3) M). Our results provide an additional explanation for the mechanism underlying the actions of cyproheptadine as an antiarrhythmic and an antipruritic agent.

Action Potentials↗

PubMed1979

Ingestive behavior and composition of weight change during cyproheptadine administration.

The effect of cyproheptadine on spontaneous energy intake was studied by means of an automated (liquid diet) food-dispensing apparatus in two nonobese adults confined to a metabolic ward. The experimental design included both single and double-blind periods. Throughout, the composition of daily weight change was determined by the energy-nitrogen balance method. While on cyproheptadine, both subjects exhibited increases in energy intake with the following average composition of weight gain: protein 16%, fat 14% and water 70% (first subject), and protein 5%, fat 49% and water 46% (second subject). The cyproheptadine-induced increase in energy intake was statistically significant in one of the subjects, who was at his desirable weight level at the outset. The other subject was underweight initially and tended to gain throughout the experiment, although rate of weight gain appeared to be more rapid during the periods of cyproheptadine administration. Energy output in both subjects remained fairly constant throughout. We conclude that cyproheptadine induces weight gain of 'normal' composition by stimulating increased energy intake.

Adult↗

PubMed1977

Suppression of human growth hormone secretion by cyproheptadine.

In order to determine whether or not a serotoninergic mechanism is involved in the secretion of the growth hormone (GH), a study was made of the effect of cyproheptadine, an antiserotonin agent, on plasma GH levels in normal children. The oral administration of cyproheptadine (12 mg daily) reduced GH responses to both L-dopa and glucagon; similarly, the mean GH response to oral glucose administration was significantly reduced after cyproheptadine administration. Plasma glucose values during the tests were not altered by cyproheptadine therapy. These results suggest that the serotoninergic mechanism might be involved in L-dopa-, glucagon-, and glucose-induced GH release.

Child↗

PubMed1979

The effect of cyproheptadine on the release of corticotrophin releasing factor.

The effect of cyproheptadine was tested on the neurotransmitter-induced release of corticotrophin releasing factor (CRF) from the rat hypothalamus in vitro. It was found that cyproheptadine inhibited both acetylcholine and 5-hydroxytryptamine-induced release of CRF. Cyproheptadine did not interfere with the ACTH releasing ability of CRF. These results suggest that cyproheptadine reduces the high circulating levels of ACTH in some patients suffering from Cushing's disease and Nelson's syndrome by inhibiting CRF secretion.

Acetylcholine↗

PubMed1976

Inhibition o'f insulin release by cyproheptadine: effects on 3',5'-cyclic-AMP-content and 45Ca-accumulation of incubated mouse islets.

Cyproheptadine (1, 10 and 100 muM) significantly reduced insulin release from isolated mouse islets in response to glucose. In contrast, 1 mM cyproheptadine induced a large release of insulin into the incubation medium probably due to islet cell damage, since the islets had lost a considerable amount of their protein content. 3',5'-cyclic-AMP-levels of the islets were not significantly affected by 10 muM cyproheptadine in the presence as well as in the absence of theophylline (10 mM). As the inhibitory effect of cyproheptadine on insulin release was correlated with reduced accumulation of calcium-45, the agent may inhibit insulin release by interfering with the calcium handling of the beta-cell.

Animals↗

PubMed1979

Cyproheptadine in the management of the galactorrhea-amenorrhea syndrome.

We evaluated long-term treatment with the antiserotonergic agent cyproheptadine in the management of the galactorrhea-amenorrhea syndrome. Fifteen women with a mean initial serum prolactin of 37 +/- 7 ng/mL received 16 to 24 mg of cyproheptadine daily; they had a significant decrease in prolactin concentration at 8 and at 16 weeks (P less than 0.01). Gonadotropin responses were variable, but no significant changes were recorded during treatment. Ten of the 15 women had menstrual bleeding while receiving cyproheptadine, seven had decreased galactorrhea, and two had cessation of galactorrhea. The side effects of treatment were transient drowsiness and weight gain. We conclude that long-term treatment of the galactorrhea-amenorrhea syndrome with cyproheptadine is effective in lowering serum prolactin in patients with mildly elevated or normal levels. Its effect on fertility remains to be ascertained.

Adult↗

PubMed1976

[Transitory remission of hypercorticism by means of cyproheptadine in a patient with Cushing syndrome].

In patients with Cushing's syndrome of hypothalamischem Cushing-Syndrom wereden eine zentrale Störung und eine wichtige Rolle des Serotonins. Accordingly, in the present study a patient with hypothalamic-pituitary hypercorticism was treated with the seotonin antagonist cyproheptadine. Urinary free cortisol excretion was measured repeatedly before, during and after therapy. In addition, night-day rhythm of plasma cortisol was determined before and at the end of cyproheptadine medication. Within 2 months, therapy with 24 mg cyproheptadine resulted in a lowering of urinary cortisol excretion to normal values. Then, however, despite continuation of the therapy, urinary free cortisol excretion rates again rose to pathological levels. Due to the occurrence of severe psychosis, the drug had to be withdrawn. Before and under cyproheptadine no night-day rhythm of plasma cortisol could be observed.

Adrenalectomy↗

PubMedDate not supplied

Disposition of cyproheptadine in rats, mice, and humans and identification of a stable epoxide metabolite.

Radioactivity was excreted in the urine and feces of rats, mice, and humans after a dose of 14C-cyproheptadine. The major metabolite in rat urine was unconjugated, but the majority of radioactive materials in mouse and human urine were conjugated with glucuronic acid. Identification of the rat urinary metabolite of cyproheptadine as an epoxide was accomplished with mass spectrometry and other methods. The rat metabolite was 10.11 -epoxydesmethylcyproheptadine and accounted for about 25% of a 45-mg dose of cyproheptadine per kg. Only a small amount of this epoxide was found in mouse urine, and none was apparent in the urine of two humans who received 5 mg of the drug. Dihydrodiols, which could arise by epoxide hydrase hydrolysis of possible 10.11-epoxy metabolites, were not found in the urine of any of the species studied. The spoxide found in rat urine appears to be unusually stable to in vivo hydrolysis. Possible implications of these results in the species-selective pancreotoxicity of cyproheptadine in the rat are presented.

Adult↗

PubMed1977

Effect of indomethacin and cyproheptadine on onset of labour in rats.

An attempt was made to postpone term in 59 pregnant rats by s.c. injections of indomethacin or cyproheptadine, or a combination of both. The cyproheptadine group gave birth to their litters on days 20-22, yet indomethacin postponed labour to the 23rd day, both when given alone or in combination with cyproheptadine. As the fourth saline group went into labour on the 20--23rd day the indomethacin postponement cannot be considered significant. Indomethacin being a prostaglandin antagonist and cyproheptadine a serotinin antagonist, it may be concluded that neither prostaglandin nor serotonin are decisive for the intricate process which triggers parturition. Other factors, such as decrease of progesterone, increase of oestrogen and perhaps foetal oxytocin, as well as placental ACTH, seem to concur in inducing labour, their effect being fortified by serotonin and prostaglandins during parturition.

Animals↗

PubMed1977

Primary acquired cold urticaria. Double-blind comparative study of treatment with cyproheptadine, chlorpheniramine, and placebo.

Eight subjects with primary-acquired cold urticaria were treated with chlorpheniramine maleate, cyproheptadine hydrochloride, and placebo in a double-blind clinical trial. During three separate seven-day treatment periods, each patient took 4 mg of either active drug or lactose placebo three times a day. Objective measurements were made at the beginning and end of each treatment period by establishing the minimum time (MT) of cold stimulus application required to provoke urtication. In addition, the spontaneous appearance of cold urticaria lesions was recorded during each treatment period. The MT required for induction of urtication with a cold stimulus was significantly greater for eight patients receiving cyproheptadine as compared to chlorpheniramine or placebo (P less than .01). The study demonstrated that cyproheptadine had a significant suppressive action on experimental cold-induced urticaria, while placebo and chlorpheniramine proved ineffective.

Adolescent↗

PubMed1977

Role of the pituitary in cyproheptadine-induced pancreatic beta-cell toxicity.

Hypophysectomized rats given cyproheptadine (40 mg/kg) for 10 days exhibited a loss of pancreatic immunoreactive insulin and ultrastructural changes in the cytoplasm of beta-cells. Sham-operated animals given cyproheptadine showed identical changes in pancreatic beta-cells except that cytoplasmic involvement progressed to the formation of large vacuoles. The pituitary is not directly involved with the cyproheptadine-induced depletion of pancreatic insulin but plays a role in the formation of large cytoplasmic vacuoles.

Animals↗

PubMed1977

A comparison of the antiserotonin, antihistamine, and anticholinergic activity of cyproheptadine with analogues having furan nuclei fused to the 10,11-vinylene bridge.

A series of cyproheptadine derivatives having furan nuclei fused to the 10,11-vinylene bridge has been prepared. None of the compounds retain the potent antiserotonin and antihistaminic actions of cyproheptadine. 1-methyl-4-(1-methyl-8H-dibenzo[a,e]furo[3,4-c]cyclohepten-8-ylidene)piperidine (7), 1-methyl-4-(1,3-dihydro-1-oxo-8H-[3,4:6,7]cycloheptal[1,2-c]furan-8-ylidene)piperidine (10), and its reduction product 11 retained the peripheral anticholinergic activity of cyproheptadine.

Animals↗

PubMedDate not supplied

Inhibition of bovine cerebral cortex prostaglandin synthetase by phenoxybenzamine and cyproheptadine in vitro.

1. Bovine cerebral cortex (BCC) microsomes were isolated from fresh brain using standard techniques. 2. Two a-adrenoceptor antagonists (phenoxybenzamine and phentolamine) and two anti-serotonin compounds (cyproheptadine and cinanserine) were compared with the anti-inflammatory drugs indomethacin and keptoprofene for inhibition in vitro of prostaglandin (PC) synthetase. 3. Henoxybenzanine and cyproheptadine inhibited BCC PG synthetase in vitro, but their potency was 1% that of indomethacin and keptoprofene. Phentolamine and cinanserine did not inhibit PG synthetase in concentrations up to ten times the effective concentrations of the other test drugs. 4. It is suggested that the antipyrogenic effect of phenoxybenzamine and cyproheptadine may be due to their inhibitory effect on prostaglandin synthesis.

Animals↗