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Periactin (Cyproheptadine)
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Periactin

Generic Periactin is used to relieve cold- and allergy-related symptoms such as hay fever, nasal inflammation, stuffy nose, red and inflamed eyes, hives, and swelling. Generic Periactin is approved by FDA. Generic Periactin blocks the effects of the naturally occurring chemical histamine in your body.

Other names for this medication:

Similar Products:
Atarax, Phenergan, Flonase, Allegra

 

Also known as:  Cyproheptadine.

Description

Generic Periactin is used to treat fever, nasal inflammation, stuffy nose, red and inflamed eyes, hives, swelling and other symptoms of cold and allergy.

Generic Periactin blocks the effects of the naturally occurring chemical histamine in your body.

Periactin is also known as Cyproheptadine, Ciplactin, Periactine, Ciproral.

Generic name of Generic Periactin is Cyproheptadine.

Brand name of Generic Periactin is Periactin.

Dosage

Generic Periactin can be taken in tablets (4mg) and syrup. You should take it by mouth.

Take Generic Periactin by mouth with or without food.

Measure the syrup form of Generic Periactin with a special dose-measuring spoon or cup.

If you want to achieve most effective results do not stop taking Generic Periactin suddenly.

Overdose

If you overdose Generic Periactin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Periactin overdosage: extreme sleepiness, confusion, weakness, ringing in the ears, blurred vision, large pupils, dry mouth, flushing, fever, shaking, insomnia, hallucinations, seizure.

Storage

Store at room temperature between 15 to 30 degrees C (59 to 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Periactin are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Periactin if you are allergic to Generic Periactin components.

Try to be careful with Generic Periactin if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Periactin can harm your baby.

Do not take cyproheptadine if you have taken a monoamine oxidase inhibitor (MAOI) such as isocarboxazid (Marplan), phenelzine (Nardil), or tranylcypromine (Parnate) in the last 14 days.

Be careful in taking Generic Periactin if you have glaucoma or pressure in the eye, stomach ulcer, enlarged prostate, bladder problems, difficulty urinating, hyperthyroidism, hypertension, any problems with heart, asthma.

Be careful with taking Generic Periactin if you use anxiety or sleep medicines such as alprazolam (Xanax), diazepam (Valium), chlordiazepoxide (Librium), temazepam (Restoril), or triazolam (Halcion); anti-depression medications such as amitriptyline (Elavil), doxepin (Sinequan), nortriptyline (Pamelor), fluoxetine (Prozac), sertraline (Zoloft), or paroxetine (Paxil); any other medications that make you feel drowsy, sleepy, or relaxed.

Avoid machine driving while taking Generic Periactin.

Avoid alcohol.

Do not stop taking Generic Periactin suddenly.

periactin generic

The intracerebroventricular administration of carbachol chloride induced a characteristic wet dog shake response in rats. Neither 5,6-dihydroxytryptamine, a serotonergic depletor, nor DL-p-chlorophenylalanine, an inhibitor of 5-HT synthesis, affected wet dog shakes induced by carbachol. Putative antiserotonergic drugs such as cyproheptadine, danitracen and pizotifen antagonized carbachol-induced wet dog shakes, but the 5-HT-receptor antagonist methergoline did not significantly affect the response. These results indicated that carbachol-induced wet dog shakes in rats are probably not related to increased activity of central serotonergic mechanisms. Additionally, the present experiments showed that the anticholinergic properties of the potent serotonergic blockers cyproheptadine, danitracen and pizotifen must be taken into account, and these drugs should be used with care as relatively selective pharmacological tools.

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Comparison of the serotonin 5-HT2A receptor affinities of a parallel series of structural analogues of the novel ligand 9-aminomethyl-9,10-dihydroanthracene (AMDA) and a structurally similar prototypical tricyclic amine cyproheptadine suggests that the two agents bind to the receptor in different fashions. Examination of ligand-receptor model complexes supports the experimental data and suggests a potential origin for the differences in binding modes.

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Pancreatic islet cell vacuolization, hyperglycemia, and glucose intolerance develop in rats after oral administration of cyproheptadine (CPH). In order to determine whether these effects were associated with abnormal insulin secretion, pancreas segments from CPH-treated and control rats were compared for their ability to secrete insulin in response to several stimuli. Oral administration of CPH (45 mg/kg/day) to rats for 1 or 8 days inhibited glucose-mediated insulin secretion from pancreas segments obtained 3 and 24 hr after the last dose of the drug. Insulin secretion had returned to normal by 48 hr after drug administration. Intraperitoneal administration of the drug was less effective than oral administration in inhibiting in vitro insulin secretion. Other stimuli for insulin secretion (tolbutamide, glucagon, L-leucine, and dibutyryl 3',5'cyclic AMP), like glucose, were incapable of releasing normal amounts of insulin from pancreas segments of CPH-treated rats. CPH and a metabolite, desmethyl-CPH, inhibited glucose-stimulated insulin secretion when added in vitro to pancreas segments from control rats. This suggests that the inhibition of insulin secretion in pancreas segments taken from animals treated with CPH could be due, at least in part, to the presence of drug and its metabolite in the tissue. A previously observed reduction in the pancreatic content of insulin in CPH-treated rats may also contribute to the abnormal insulin release in animals given the drug.

periactin dosage children

Levocetirizine, the active enantiomer of cetirizine, is more potent and consistent than other popular H1 antihistamines for blocking the cutaneous response to histamine. These findings may predict the efficacy of this drug in treating allergic disorders.

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Mast cells have been linked to rheumatoid arthritis (RA) and are essential to the pathogenesis of RA-like disease in a mouse model. We describe a 34-year-old woman who developed Sjögren's syndrome concurrently with telangiectasia macularis eruptiva perstans (TMEP), a rare form of cutaneous mastocytosis. The patient had sicca symptoms with an abnormal minor salivary gland biopsy and decreased salivary flow, peripheral neuropathy, an 80 pound weight loss, and a macular erythematous rash that exhibited superficial perivascular mast cell infiltrates on biopsy of lesional skin. This case further underscores the link between mast cells and the development of autoimmunity.

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The association between adenoidal hypertrophy and rhinosinusitis with upper airway inflammation is increasingly recognized; however, no study has used magnetic resonance imaging (MRI) to assess the changes in adenoid size after medical treatment of rhinosinusitis.

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In patients with perennial allergic rhinitis, vitamin E supplementation (400 IU/d) did not have any significant effects on nasal symptom severity or on serum concentrations of specific IgE to 5 common allergens.

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Loratadine syrup disrupted normal urethral development in the mouse, based on gross morphology and histological assessment, and also disrupted steroid receptor expression, producing an expression profile similar to that resulting from in utero exposure to ethinyl estradiol.

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In total, 20 adult Sprague-Dawley rats were used in this study. An ovalbumin-induced allergic rhinitis model was formed in three study groups except for the control group. Bosentan (100 mg/kg/day) was given to the bosentan-treated group for 7 days and desloratadine (10 mg/kg/day) was administered to the antihistaminic-treated group for 7 days. Nasal symptom scorings and histopathological examinations of the nasal tissues were carried out. Serum IgE levels and ET-1 and TNF-alpha mRNA expression levels were analysed. Between group comparisons for nasal symptoms, histopathological analysis, and molecular analyses were performed with a one-way ANOVA and Duncans multiple comparison tests. Significance was accepted at p smaller than 0.05.

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Limited information is available regarding sedation and motor function following repeat dosing of antihistamines. This study examined how promethazine and loratadine affect day-time drowsiness, the commencement of voluntary movement, and involuntary movement when administered on consecutive days.

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The effects of third ventricle (3V) infusion of exogenous monoamines on the secretion of LH were investigated in Nembutal-blocked proestrous rats after electrochemical stimulation (ECS) of the medial preoptic area (MPOA). Two microcannulae were anatomically oriented through the ventral surface of the brain to establish a push-pull flow system in the 3V at the rate of 3.9 microliter/min for 160 min. Serotonin perfusions (2.6 x 10(-3) M for 160 min at 3.9 microgram/min) significantly depressed the MPOA-ECS-induced rise in plasma LH at 160 and 200 min, but did not diminish the secretion of LH after an intraatrial injection of 250 ng LRH. Seemingly, the reduced plasma LH which follows MPOA-ECS in serotonin-treated rats is the consequence of decreased hypothalamic LRH secretion. Desipramine (3.6 x 10(-4) M), a norepinephrine (NE) uptake inhibitor, did not prevent serotonin inhibition. In contrast, the specific serotonin uptake inhibitor. Lilly 110140 (3.2 X 10(-4) M), and cyproheptadine (2.9 x 10(-4) M) blocked the inhibitory effects of serotonin. Serotonin was also tested in proestrous rats anesthetized with Nembutal within 1 h after the beginning of the light cycle (morning rats) and in proestrous rats at least 15 min after the start of the dark cycle (night rats). Serotonin (2.6 x 10(-3) M) failed to diminish the rise in plasma LH after ECS in morning rats, but depressed the ECS-induced increase of LH in night rats. Perfusions of 3 X 10(-8) M NE at 3.9 microliter/min for 160 min augmented the plasma LH increase after MPOA-ECS but only at 160 and 200 min, while its response to LRH was not tested. At higher concentrations, 3 x 10(-6) M NE markedly suppressed the rise in plasma LH after ECS and also depressed the secretion of LH after an intraatrial injection of LRH. In contrast, 3 x 10(-6) M epinephrine which inhibited the response to LRH, potentiated the MPOA-ECS-induced rise in plasma LH. Higher concentrations of epinephrine (3 x 10(-4) M), however, inhibited both the ECS and LRH-induced secretion of LH.

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Release of plasma ACTH- and beta-endorphin (beta-EP)-like immunoreactivity (LI) was studied in vivo in a patient with an ectopic ACTH-producing malignant thymoma. Administration of lysin vasopressin stimulated concomitant release of plasma ACTH- and beta-EP-LI. Administration of cyproheptadine, naloxone, and somatostatin significantly suppressed plasma levels of ACTH- and beta-EP-LI, while saline infusion did not. Gel exclusion chromatography of the plasma extracts revealed that ACTH-LI consisted of two components, large and small molecular weight form, while beta-EP-LI consisted of three components, large molecular weight, beta-lipotropin-, and beta-EP-sized form; each of these components was incompletely suppressed by somatostatin infusion. It is suggested that certain tumors may have acquired aberrant multiple receptors during malignant transformation which may lead to the paradoxical hormone response as demonstrated in this case.

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Rats pretreated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 10 micrograms/kg) are supersensitive to the edemagenic effects of carrageenan and dextran as indicated by the increased potency of these irritants in TCDD-treated animals compared to controls. This effect of TCDD was characterized using indomethacin, dexamethasone and a combination of cyproheptadine and pyrilamine as inhibitors of edema formation. Because TCDD increases the potency of carrageenan and dextran, it was necessary to select appropriate doses of the edemagenic irritants in order to evaluate the effect of edema inhibitors properly. At low and moderate irritant doses, TCDD-treated and control rats exhibited similar responses to inhibitory agents, suggesting that the mechanisms by which carrageenan and dextran produce edema involve the same mediators in control and TCDD-treated animals. The effect of TCDD on edema induced by bradykinin, histamine, prostaglandin E2 and serotonin, substances which are postulated endogenous mediators of carrageenan-, dextran- and/or compound 48/80-induced edemas, was also examined. Inasmuch as TCDD increased the edemagenic potency of bradykinin and histamine, but not that of prostaglandin E2 or serotonin, it was concluded that TCDD enhances carrageenan-, dextran- and compound 48/80-induced edema formation by augmenting the edemagenic activities of bradykinin and histamine. It is postulated that the mechanism of enhancement may involve TCDD-induced potentiation of the ability of bradykinin and histamine to stimulate phospholipase activity in vascular endothelial cells.

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Prazosin is recommended for treatment of Posttraumatic Stress Disorder (PTSD)-associated nightmares. Level A. Image Rehearsal Therapy (IRT) is recommended for treatment of nightmare disorder. Level A. Systematic Desensitization and Progressive Deep Muscle Relaxation training are suggested for treatment of idiopathic nightmares. Level B. Venlafaxine is not suggested for treatment of PTSD-associated nightmares. Level B. Clonidine may be considered for treatment of PTSD-associated nightmares. Level C. The following medications may be considered for treatment of PTSD-associated nightmares, but the data are low grade and sparse: trazodone, atypical antipsychotic medications, topiramate, low dose cortisol, fluvoxamine, triazolam and nitrazepam, phenelzine, gabapentin, cyproheptadine, and tricyclic antidepressants. Nefazodone is not recommended as first line therapy for nightmare disorder because of the increased risk of hepatotoxicity. Level C. The following behavioral therapies may be considered for treatment of PTSD-associated nightmares based on low-grade evidence: Exposure, Relaxation, and Rescripting Therapy (ERRT); Sleep Dynamic Therapy; Hypnosis; Eye-Movement Desensitization and Reprocessing (EMDR); and the Testimony Method. Level C. The following behavioral therapies may be considered for treatment of nightmare disorder based on low-grade evidence: Lucid Dreaming Therapy and Self-Exposure Therapy. Level C No recommendation is made regarding clonazepam and individual psychotherapy because of sparse data.

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Recently, it is claimed that the usage of the intranasal glucocorticosteroids alone, instead of H1-antihistamines + intranasal glucocorticosteroids, reduces the complaints in moderate-to-severe seasonal allergic rhinitis (SAR). This study aims to evaluate the efficacy of the intranasal glucocorticosteroids alone during the pollen season by using objective and subjective parameters. Twenty-four patients (mean age, 12.17 +/- 2.26 years) with SAR sensitive to pollen are included in this study. The patients were divided into two groups randomly. Twelve patients in group I were given H1-antihistamine (loratadine) + intranasal glucocorticosteroid (mometasone furoate), and 12 patients in group II were given only intranasal glucocorticosteroid (mometasone furoate) for 12 weeks. To evaluate the results, subjective parameters (daytime nasal symptoms score, daytime eye symptoms score, and nighttime symptoms score) and objective parameters (nasal smear, nasal peak inspiratory flow [NPIF], and nasal biopsy) are used. With regard to the baseline data, it was observed that both groups had a significant decrease in total symptom score (p < 0.01), a significant increase in NPIF values (p < 0.01), and a significant decrease in the number of eosinophils in both nasal smear and biopsy (p < 0.01) after treatment. Comparing groups I and II in terms of treatment success, the improvement in daytime nasal symptoms score (p < 0.01 versus p < 0.01), daytime eye symptoms score (p < 0.01 versus p < 0.01), and total symptom score (p < 0.versus p < 0.01) was not different. However, there was a significant improvement in nighttime symptoms score between groups I and II (p < 0.01 versus p > 0.05). Furthermore, NPIF and nasal biopsy findings did not differ between groups (p > 0.05). The usage of H1-antihistamine + intranasal glucocorticosteroid has no superiority over the administration of intranasal glucocorticosteroid alone for treatment of SAR in pollen season. However, this finding needs to be confirmed in larger series studies.

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The influence of various 5-hydroxytryptaminergic agonist and antagonist drugs on body-temperature response to cobaltous chloride in mice was noted. Pretreatment with p-chloroamphetamine, p-chlorophenylalanine, and p-iodoamphetamine antagonized the body-temperature response to cobalt. p-Chloroamphetamine and p-chlorophenylalanine reduced, while p-iodoamphetamine elevated, brain serotonin levels. The uptake inhibitor agents, fluoxetine and nisoxetine, failed to modify the ability of p-chloroamphetamine to antagonize cobalt hypothermia. Cyproheptadine, methergoline, and xylamidine pretreatment enhanced rather than antagonized body-temperature depression by cobalt. Tryptophan hydroxylase inhibitors antagonized cobalt hypothermia, but receptor-blocking agents were without influence, indicating that antagonism was mediated through mechanisms other than the depletion of serotonin. Elevation rather than depletion of brain serotonin by p-iodoamphetamine and failure of uptake inhibitors to modify p-chloroamphetamine antagonism of cobalt hypothermia lend further support for a nonserotonergic role of these amines in their ability to antagonize body-temperature depression by cobaltous chloride in mice.

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Thirty-five patients with moderate-to-severe asthma, most receiving inhaled steroids, were enrolled in this double-blind, crossover study. In addition to their maintenance therapy patients received either loratadine, 20 mg once daily, or placebo for 4 weeks before crossing over to the other preparation for a further 4 weeks. Variables of efficacy were daily and nocturnal respiratory symptoms, lung function (PEF, FEV1, FVC), and bronchodilator use.

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Influence of GABA onlocomotor activity and gross behavior of mice, rats, and rabbits was studied. In mice and rats, IP GABA injection produced decreased locomotor activity, but in rats and rabbits head twitches and disturbances in body balance were seen. GABA-induced head twitches were inhibited by picrotoxin, clonidine, morphine, or cyproheptadine. Our results suggest a serotonergic component in GABA-induced head twitches, but it is not the only mechanism involved in this behavior.

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This study investigated the additive effects of concomitant montelukast and loratadine when compared with montelukast, loratadine, and inhaled beclomethasone monotherapies in asthma. Methods. Patients (N = 406) were 15 to 65 years of age with a forced expiratory volume in 1 second (FEV(1))-predicted of 50% to 85%, FEV(1) reversibility > or = 15%, and a minimal level of daytime symptoms and beta -agonist use. This three-part 2X2 crossover-study consisted of two double-blind 6-week treatment periods where patients were administered once daily oral montelukast 10 mg, loratadine 10 mg, montelukast 10 mg + loratadine 10 mg, or twice daily inhaled beclomethasone 200 mu g. A subsequent 48-week extension study compared montelukast + loratadine with beclomethasone. The primary endpoint was the percentage change from baseline in FEV(1).

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A survey of novel small-molecule therapeutics reveals that the majority of them result from analogue design and that their market value represents two-thirds of all small-molecule sales. In natural science, the term analogue, derived from the Latin and Greek analogia, has always been used to describe structural and functional similarity. Extended to drugs, this definition implies that the analogue of an existing drug molecule shares structural and pharmacological similarities with the original compound. Formally, this definition allows the establishment of three categories of drug analogues: analogues possessing chemical and pharmacological similarities (direct analogues); analogues possessing structural similarities only (structural analogues); and chemically different compounds displaying similar pharmacological properties (functional analogues).

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Intracerebral (i.c.) injection of serotonin (5-HT) into mice induced head twitches in a dose-dependent manner at 10 min after injection. The head twitches induced by 5-HT (i.c.) were potentiated by the pretreatment of isocarboxazid (3 mg/kg i.p.), and inhibited by cyproheptadine (0.3 mg/kg i.p.), a 5-HT antagonist. Benzodiazepines such as fludiazepam and diazepam potentiated the head twitches induced by 5-HT (i.c.) in a dose-dependent manner. Mescaline (50 mg/kg i.p.) also induced head twitches in mice at 15 and 30 min after injection. Benzodiazepines potentiated the head twitches induced by mescaline in a dose-dependent manner. Cyproheptadine blocked the potentiating effect of benzodiazepines on the head twitches induced by both 5-HT (i.c.) and mescaline. By repeated administration of fludiazepam or diazepam for 5 days, the potentiating effect of both drugs on the head twitches induced by mescaline was unchanged and their anticonvulsant effects were not modified. In contrast, the potency of both drugs on muscle relaxation was significantly decreased by repeated administration. Benzodiazepines failed to change the uptake of 5-HT into the synaptosomal fractions from the rat brain. These results suggest that the pharmacological action of benzodiazepines is derived at least in part from their activating effect on 5-HT receptors.

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A randomized, double blind, parallel-group, placebo-controlled study was carried out in patients aged older than 12 years with PER. Main inclusion criteria were: instantaneous total symptom score (i6TSS) >or=45, nasal obstruction score or=2 as moderate during the first visit. The primary efficacy endpoint was the 12-week average change from baseline of the patients' i6TSS.

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Crinum glaucum A. Chev (Amaryllidaceae) (CG) is a bulbous plant widely used in folk medicine in the treatment of cough, asthma and convulsions. This study was carried out to investigate the anticonvulsant, anxiolytic and hypnotic effects of the aqueous bulb extract of C. glaucum and its possible mechanism (s) of action. The anticonvulsant activity of C. glaucum extract (400-1200 mg kg(-1) p.o.) was investigated using picrotoxin, strychnine, isoniazid, pentylenetetrazol and N-methyl-D-aspartate (NMDA)-induced seizures in mice while the elevated plus maze test (EPM) and hexobarbitone-induced sleeping time (HIST) were used to evaluate the anxiolytic and hypnotic effects, respectively. Animals were pretreated with flumazenil (3 mg kg(-1); i.p. GABA(A) receptor antagonist), cyproheptadine (4 mg kg(-1); i.p. 5-HT2 receptor antagonist), L-arginine (500 mg kg(-1); p.o. Nitric Oxide (NO) precursor) and L-Nitroarginine (L-NNA) (10 mg kg(-1) i.p. Nitric Oxide Synthase (NOS) inhibitor) were used to investigate the probable mechanism (s) of anticonvulsant activity. Oral administration of CG significantly (p < 0.001) delayed the onset of seizures induced by picrotoxin, strychnine, isoniazid and pentylenetetrazol with peak effect at 1200 mg kg(-1) in comparison to control groups. CG (800 and 1200 mg kg(-1)) strongly antagonized NMDA-induced turning behavior. Pretreatment of mice with cyproheptadine could not reverse the anticonvulsant effect of CG. However, pretreatment with flumazenil and L-NNA significantly (p < 0.05) reversed the anticonvulsant effect of CG while L-arginine pretreatment significantly (p < 0.001) delayed the onset of seizures when compared with control and extract (1200 mg kg(-1) only). CG potentiated hexobarbitone-induced sleeping time with peak effect at 400 mg kg(-1) and also significantly (p < 0.05) increased open arm exploration in EPM and had its peak anxiolytic effect at 100 mg kg(-1). The data obtained suggests that aqueous bulb extract of Crinum glaucum possess anticonvulsant, anxiolytic and hypnotic activities which involve an interaction with GABAergic, nitrergic and glutaminergic systems to exert its effects.

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periactin buy 2015-08-06

The effects of cyproheptadine on basal and glucose-induced insulin release by isolated rat islets was studied by use of a perifusion system. A forty-five minute preincubation of islets with a medium containing both 34.3 mug./ml. (10(-4) M) cyproheptadine and 1.0 mg./ml. glucose completely abolished the biphasic pattern of increased insulin secretion normally obtained after islets are stimulated with a medium containing 3.0 mg./ml. glucose. In another series of experiments, similar results were obtained when the cyproheptadine and 3.0 mg./ml. glucose were presented together. Here, however, the inhibition of the first phase of insulin secretion did not achieve statistical significance and some recovery of the islets' secretory capacity was buy periactin online observed late during the second phase. In studies designed to investigate the influence of cyproheptadine on basal insulin secretion, no obvious effect was observed. These results are discussed in relation to the species-specific alterations in pancreatic beta-cell morphology that have been reported in rats after the oral administration of cyproheptadine.

periactin migraine reviews 2016-01-15

There is growing interest in investigating the role of 5-HT receptors in the physiopathology of schizophrenia in particular the negative symptoms. Indeed, buy periactin online newer atypical antipsychotics which interact with 5-HT receptors are more effective in the treatment of negative symptoms compared to typical neuroleptics. We undertook a trial to investigate whether the combination of haloperidol with cyproheptadine, a relatively safe serotonin-blocking agent was more effective than haloperidol alone.

periactin overdose 2016-01-12

The aim of this study is to determine whether montelukast, a LTD4 receptor antagonist, plus desloratadine, buy periactin online is more efficacious than desloratadine alone in the treatment of chronic urticaria.

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The National Libraray of Medicine buy periactin online was searched for current data of the effects of histamine and antihistamines in allergic rhinitis.

periactin generic 2017-01-04

Exposure of conscious young rats to 4 h heat stress at 38 degrees C in B.O.D. incubator was associated with increased blood-brain barrier (BBB) permeability in 14 brain regions studied. In the same regions cerebral flow (CBF) diminished by 4- buy periactin online 65%, but the magnitude of flow reduction was not correlated with the degree of increased BBB permeability. On the other hand, a correlation was observed with increased plasma and brain 5-hydroxytryptamine (5-HT) levels. p-Chlorophenylalanine (p-CPA), indomethacin and diazepam pretreatment prevented both the increased BBB permeability and 5-HT levels following heat exposure. Whereas cyproheptadine and vinblastine pretreatment prevented the increased BBB permeability alone. The probable mechanism(s) underlying the BBB permeability is discussed.

periactin 4mg dose 2017-02-11

This study aimed to investigate whether the single nucleotide polymorphisms (SNPs) in C5AR1 are associated with CSU susceptibility and antihistamines therapeutic efficacy in Chinese buy periactin online CSU patients.

periactin pediatric dosage 2015-08-08

Allergic rhinitis afflicts close to 40% of the nation's population and costs more than $1.8 billion a year. The toll exacted by this disorder has been greatly alleviated by nonsedating second-generation antihistamines loratadine, terfenadine, and astemizole. The three agents effectively reduce symptoms without the sometimes intolerable adverse effects of older drugs, but they are not completely equivalent. For example, terfenadine requires twice/day dosing, whereas the others can be given once/day. Astemizole has a slow onset and extremely prolonged duration of action. Both terfenadine and astemizole may have cardiotoxic effects (e. buy periactin online g., torsades de pointes) when serum concentrations rise due to overdosing or drug interactions. Cetirizine, a recently approved second-generation antihistamine, has sedative and anticholinergic effects, although to a lesser degree than the first-generation antihistamines.

periactin dosage pediatric 2017-09-09

The aim of the study was to develop intraoral films (IOFs) of loratadine and to assess the storage conditions by dynamic vapour sorption studies. The excipient selection was guided by drug excipient compatibility studies and the incompatibility of loratadine with dibutylphathalate and Tween20 was confirmed by Electro-spray Ionization Mass Spectrometry. Thus intaroral films were developed using HPMC E-15 LV and polyvinyl alcohol (PVA) as lone and mixed film formers to get eighteen formulations (F1- F18) that varied in the type and amount of plasticizer used. Four formulations selected on the basis of pharmacotechnical characteristics were improvised by inclusion of Poloxamer407 that lowered the dissolving time to the tune of 36-55%. Dynamic vapour sorption studies of the improvised films (PF1-PF4) demonstrated an increase of 2% by weight at 50% relative humidity (RH) and 25°C suggesting storage of the films below the stated conditions. In vitro drug release studies in buy periactin online phosphate buffer pH 6.8 demonstrated more than 94% cumulative drug release from the formulations. Analysis of model independent parameters identified PF2 as the best formulation that was nine times superior in its dissolution efficiency to Lorafast tablets(®).

periactin vita syrup 2017-11-06

A patient with Cushing's disease failed to show complete suppressibility of adrenal function with conventional "high" doses of dexamethasone (8 mg per day). Higher doses were required to achieve suppression. Pituitary irradiation and medical therapy (cyproheptadine, metyrapone, and aminoglutethimide) failed to control the disease, necessitating bilateral adrenalectomy. The diagnostic and therapeutic implications of megadose dexamethasone suppression have buy periactin online not been clearly addressed in the medical literature. It is possible that adrenal suppression achieved only with unconventionally high doses of steroids may be predictive of refractoriness to nonsurgical therapy.

periactin purchase 2016-03-16

The synthesis and orexigenic activity of some unsubstituted and Bz-carboxylic acid substituted 1-methyl-4-piperidylidenepyrrolo[2,1-b][3]benzazepine and dibenzocycloheptene derivatives are described. 10,11-Dihydro-3-carboxycyproheptadine (7c) has been selected for clinical evaluation as a orexigenic agent based on its low threshold dose for increasing food consumption in cats (0.031 mg/kg po) and its lack of undesirable central nervous system activity. The levorotatory enantiomer of 3-carboxycyproheptadine (1d) and the 9-carboxypyrrolobenzazepine derivative 4f also possess orexigenic activity, but with these compounds such activity diminishes sharply below 0.25 mg/kg po. The unsubstituted 1-methyl-4-(5H-pyrrolo[2,1-b][3]benzazepin-11-ylidene)piperidine (4d) and its 6,11-dihydroanalogue (4a) are comparable to cyproheptadine (1a) in promoting hyperphagia buy periactin online in cats.

periactin 4mg tablets 2016-07-06

The improvement of nasal symptoms in patients with AR treated with buy periactin online antihistamines, with or without montelukast, may additionally result from the reduction of sICAM-1 and nasal eosinophilia. Because the combination therapy may bring inconclusive benefits in this area there is a strong need of further studies to find mechanisms that favor combination therapy.

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Weight and height velocities and IGF-I z- buy periactin online scores during cyproheptadine therapy were significantly greater in the intervention group than those of the placebo group.

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To establish an buy periactin online HPLC-fluorescence method for determination of loratadine in human plasma and evaluate its relative bioavailability.

periactin syrup dosage 2017-10-18

Placebo, montelukast, desloratadine and levocetirizine significantly improved quality of life. Combining montelukast with either levocetirizine or desloratadine gave buy periactin online additional benefits in comparison to each agent alone and could be considered for patients whose quality of life is impaired by persistent allergic rhinitis.

periactin liquid medication 2017-04-18

Comparable maximum corrected QT (QT(c)) intervals were observed after coadministration of desloratadine and placebo or ketoconazole (431 and 435 msec, respectively). The desloratadine/ketoconazole combination did not induce any statistically significant or clinically relevant changes in QT(c), QT, PR or QRS intervals compared with desloratadine alone; ventricular rate was slightly slower when desloratadine was given with ketoconazole. At steady state, coadministration of Voltaren 750 Mg ketoconazole resulted in no significant change in area under the desloratadine concentration-time curve (AUC) from 0 to 24 hours compared with desloratadine/placebo. Coadministration of desloratadine and ketoconazole resulted in a 1.3-fold increase in desloratadine maximum concentration (C(max)) that was not clinically relevant. The most common adverse event was headache, reported in 42 and 38% of individuals, respectively, after coadministration of desloratadine/placebo and desloratadine/ketoconazole. There were no reports of dizziness or syncope.

periactin 2mg tablets 2015-08-23

Ebastine is a long-acting, second-generation, selective histamine H1-receptor Celexa 10mg Cost antagonist. A fast-dissolving tablet formulation of ebastine has been developed at 10- and 20-mg doses, with the intention of facilitating administration to patients experiencing problems with swallowing, including those confined to bed and elderly people, as well as those who may need to use ebastine when they do not have easy access to water to aid swallowing a tablet.

periactin generic name 2017-07-04

To determine the selectivity of the non-sedating antihistamines loratadine and terfenadine and the sedating antihistamine diphenhydramine for peripheral and central histamine H1-receptors, these compounds were examined against intravenous (i.v.) and intracerebroventricular (i.c.v.) histamine-induced bronchoconstriction in anesthetized, spontaneously breathing guinea pigs. Animals were prepared with i.c.v. or i.v. cannulas and instrumented for the measurement of airway resistance (RAW) and dynamic lung compliance (CDyN). Loratadine, terfenadine or diphenhydramine were administered orally 2 h before either i.v. or i.c.v. injection of histamine. Each antihistamine blocked the i.v. histamine bronchospasm with the order of potency loratadine (ED40 = 0.08 mg/kg) greater than terfenadine (ED40 = 0.44 mg/kg) greater than diphenhydramine (ED40 = 5 mg/kg). These drugs also blocked i.c.v. histamine-induced bronchoconstrictions, but loratadine and terfenadine were approximately 10 times Motilium 40 Mg less potent against i.c.v. histamine bronchoconstriction than they were against i.v. histamine. In contrast, diphenhydramine was equipotent against i.c.v. and i.v. histamine bronchoconstriction. These results demonstrate that the non-sedating antihistamines loratadine and terfenadine, unlike diphenhydramine, are more effective against peripheral than central H1-receptors, probably because of poor penetration of the blood-brain barrier.

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Mice were subjected either to repeated, intranasal application of Af extract or to intraperitoneal immunization with OVA, followed by inhalation challenge. DL or a control fluid was given Arava 40 Mg daily throughout the sensitization process. Immunoglobulin E (IgE) levels, bronchoalveolar lavage-fluid cytokines and cytology, lung histology, and physiologic responses to methacholine were assessed in the allergen-treated mice. Anti-OVA IgE responses and OVA-driven T-cell cytokine production were examined.

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Our study demonstrates the advantages of cardiac myocytes over heterologously expressed hERG channels in predicting QT interval prolongation and TdP in man. The potencies of some drugs in cardiac myocytes were similar to hERG, but only myocytes were able to detect important changes in APD characteristics and display EADs predictive of arrhythmia development. We observed similar qualitative drug profiles in cardiac myocytes, dog Purkinje fibers, and animal and human telemetry studies. Therefore, isolated native cardiac myocytes are a better predictor of drug-induced QT prolongation and TdP than heterologously Indocin Reviews expressed hERG channels. Isolated cardiac myocytes, when used with high-throughput patch clamp instruments, may have an important role in screening potential cardiotoxic compounds in the early phase of drug discovery. This would significantly reduce the attrition rate of drugs entering preclinical and/or clinical development. The current kinetics and amplitudes of the cloned hERG channel were profoundly affected by temperature, significantly altering the potency of one drug (E-4031). This finding cautions against routine drug testing at room temperature compared to physiologic temperature when using the cloned hERG channel.

periactin cyproheptadine tablets 2016-06-10

A single, 10 ng intradermal injection of human Prevacid Suspension recombinant interleukin-1 beta (rIL-1 beta) into rat ears produced acute inflammation. Tissue wet weight (edema) and total myeloperoxidase activity (PMN accumulation), peaked at 3 hours and returned to base line at 3 days. Given orally, 1 hour prior to rIL-1 beta injection, cyproheptadine, dexamethasone, conventional NSAID's, or mixed cyclooxygenase/lipoxygenase inhibitors were potent antagonists of edema and moderate antagonists of PMN accumulation. In addition, the putative DMARD's, auranofin, dapsone, and levamisole were effective inhibitors of rIL-1 beta induced inflammation.