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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.

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This study tests the hypothesis that the ability of atypical neuroleptics to improve negative symptoms is due to 5HT-receptor antagonism and enhanced frontal lobe function. We investigated the effects of cyproheptadine (a 5HT2 antagonist) on neuropsychological tests of frontal lobe functions in chronic schizophrenic patients. Eighteen stable schizophrenic patients on depot neuroleptic medication participated in a 4-week double blind crossover study. Outcome measures were clinical symptoms rating scales, neuropsychological tests (verbal fluency, Stroop colour word task, trail making) and antisaccade eye movements. During the cyproheptadine phase statistically significant improvement was seen on Stroop colour word task, verbal fluency and Trail B tests. The ability to suppress reflexive eye movement to a target light in an anti saccade task was also significantly enhanced. The patients had low clinical ratings of negative symptoms and they were unaffected by cyproheptadine. The results indicate that 5HT2C receptors selectively modulate speed and motor control mechanisms related to frontal lobe functions but this was not associated with changes in symptoms.

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The median overall survival was 11.0 months (95% confidence interval: 6.8-15.1 months) in the combination group compared with 4.8 months (95% confidence interval: 3.1-6.6 months) in the control group (crude hazard ratio = 0.45, 95% confidence interval: 0.22-0.82). The median progression-free survival time was 7.5 months (95% confidence interval: 5.1-10.0 months) in the combination group compared with 1.7 months (95% confidence interval: 1.4-2.1 months) in the control group (crude hazard ratio = 0.43, 95% confidence interval: 0.22-0.86). Kaplan-Meier survival analysis revealed that both overall survival and progression-free survival in the combination group were significantly longer than that in the control group. The multivariate model found patients in the combination group were 76% less likely to die (adjusted hazard ratio = 0.24, 95% confidence interval: 0.10-0.58) and 82% less likely to have progression (adjusted hazard ratio = 0.18, 95% confidence interval: 0.08-0.44) during the 17 months of follow-up.

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The present study adopts an ethoexperimental approach to examine the deportment subsequent to alteration in serotonin (5-HT) neurotransmission following treatment with site-specific neuropharmacological probes. The impact of perturbation in (5-HT) neurotransmission on baseline behavior was analyzed employing three animal models of anxiety, i.e., hole-board, elevated plus maze, and bright/dark arena. Inbred male rats (Wistar strain, weighing between 150 and 200 g) were used in this study. The vivarium and the behavioral laboratory were specially designed to permit operation of reversed light-dark cycle and all experiments were performed during the dark period. Pharmacological tools selected to influence 5-HT levels include (1) a combination of tranylcypromine and tryptophan (TCP + TRYPT) (0.75 mg/kg + 40 mg/kg) which augments 5-HT biosynthesis; (2) p-chlorophenylalanine (PCPA: 200 mg/kg), an inhibitor of 5-HT biosynthesis; and (3) 5-HT reuptake blockers, namely zimelidine (ZIM) (40 mg/kg) and fluoxetine (FLU) (10 mg/kg). Rats under the influence of PCPA exhibited anxiolytic response, whereas those under treatments to raise 5-HT levels, viz., TCP + TRYPT, ZIM and FLU, displayed anxiogenic-like reactions. Several other agents known to specifically interact with 5-HT receptor subtypes were also tested. 5-HT2 receptor stimulants, such as quipazine (5 mg/kg) and MK 212 (0.5 mg/kg), were found to be anxiogenic. Buspirone (2 mg/kg), a 5-HT1 agonist, surmounted normal behavioral inhibition. However, another 5-HT1 stimulant, 8-OH-DPAT (0.025 mg/kg), had anxiogenic action. Pretreatment with 5-HT3 antagonists [zacopride (2 mg/kg) and GR 38032F (0.1 mg/kg)] and putative 5-HT1 antagonist [propranolol (10 mg/kg)] resulted in borderline disinhibition of normal behavioral inhibition to novel environments. In contrast, cyproheptadine (0.5 mg/kg), a 5-HT2 antagonist, provoked anxiogenic-like behavior. Altogether, uniform results were obtained for each probe in all the three models, suggesting that the battery of anxiety tests chosen in this study is reliable and sensitive to detect unknown pharmacological responses. The results support the hypothesis that stimulation of serotonergic neurotransmission heightens normal anxiety, whereas its blockade releases normal behavioral inhibition. Furthermore, this work establishes the validity of using the three paradigms in evaluating the involvement of multiple neurotransmitter receptors in the control of behavior of rodents under natural circumstances and also detects any aberration following exposure to novelty and stress.

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Co-administration of desipramine and fluoxetine resulted in a 27% decline in cerebral cortical beta-adrenoceptor density after four days - a time point at which neither agent alone was effective. After 14 days, desipramine- and desipramine + fluoxetine-treated rats showed decreased receptor levels, with a greater decrement seen with the combined treatment. Fluoxetine, alone, had no affect on beta-adrenoceptor density at any time point examined. These effects are attributable to central serotonergic action since they were prevented by prior treatment with p-chlorophenylalanine. Cyproheptadine, a 5-HT2 antagonist, did not block these effects. Independent administration of fluoxetine and desipramine produced approximately 20% decrement in isoproterenol-stimulated cyclic AMP accumulation after four days of treatment. Co-administration of desipramine and fluoxetine resulted in a 35% decrement in cyclic AMP accumulation which was nearly additive with that produced by either drug alone. Consequently, the combination of a norepinephrine and serotonin uptake inhibitor may be an advantageous and rapid treatment for the alleviation of certain forms of depression.

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Leptin is a 167 amino acid protein encoded by the obesity gene that is synthesized in adipose tissue and interacts with receptors in the hypothalamus linked to the regulation of appetite and metabolism. It is known to suppress appetite and increase energy expenditure. Cyproheptadine is a piperidine antihistamine that increases appetite through its antiserotonergic effect on 5-HT2 receptors in the brain. Although both leptin and cyproheptadine are effective in controlling appetite, their interaction has not been addressed in clinical studies. This study evaluated serum leptin concentrations in patients who received cyproheptadine to treat a variety of disorders. Sixteen patients aged 7 to 71 years (mean, 26.25 years) were given cyproheptadine 2 to 6 mg/day for a minimum of 7 days. Body weight was measured and blood samples were obtained at baseline and after 1 week of treatment. Serum leptin levels were determined by leptin radioimmunoassay. The mean body weight at baseline (52.59 kg) did not differ significantly from that at 1 week after treatment (52.84 kg; P > .05), but the mean leptin level after 1 week of treatment with cyproheptadine (3.14 ng/mL) was 14.2% higher than that at baseline (2.75 ng/mL; P < .05). This increase may suggest that both leptin and cyproheptadine may affect appetite via similar receptors and that cyproheptadine does not impair leptin activity through these receptors. Further study will be necessary to clarify this relationship.

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In this crossover study, adults with a history of seasonal AC and a minimal threshold response to allergen challenge were randomized to receive desloratadine 5 mg daily (n=20) or placebo (n=21) for 7 days after which they underwent a second ocular allergen challenge. After a 2-week washout period, subjects crossed over to the other treatment. The primary efficacy parameter was the intra-subject difference from baseline at end-point in the post-challenge mean composite ocular redness score (the sum of redness scores in ciliary, conjunctival, or episcleral vessel beds). Secondary efficacy parameters included the intra-subject and inter-subject differences in individual symptom scores for ciliary, conjunctival, or episcleral redness; pruritus; chemosis; eyelid swelling; and tearing.

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The IC50 for rupatadine in A23187, concanavalin A and anti-IgE induced histamine release was 0.7+/-0.4 microM, 3.2+/-0.7 microM and 1.5+/-0.4 microM, respectively whereas for loratadine the IC50 was 2.1+/-0.9 microM, 4.0+/-1.3 M and 1.7+/-0.5 microM. SR-27417A exhibited no inhibitory effect. Rupatadine, loratadine and SR-27417A inhibited TNF-alpha release with IC50 2.0+/-0.9 microM, 2.1+/-1.1 M and 4.3+/-0.6 microM, respectively.

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The authors' data on time-related changes in the contractile activity of non-innervated smooth muscle amnion of the chick embryo devoid of blood vessels and on involvement of the amniotic fluid neurotransmitters in regulation of the amnion motor activity have been summarized. A scheme of possible mechanism underlying regulation of the spontaneous rhythmic contractile activity of the amnion by two antagonistic neurotransmitters present in the amniotic fluid: serotonin and noradrenalin, which stimulate and inhibit the amnion motor activity, respectively. The results of experiments on successive block of the serotonin and adrenergic receptors by introduction of the corresponding antagonists in the chick embryo amniotic fluid speak in favor of the proposed scheme of humoral regulation of the amnion motor activity. A possible involvement of this humoral mechanism in the inhibitory effect of increased carbon dioxide content of the air on the amnion motor activity has been considered.

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The aim of this study was to compare the onset of action and efficacy of the study medications.

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We conducted a 32-week, double-blind, placebo-controlled, cross-over and randomized trial that implicated two arms: arm A, 20 patients received levocetirizine, montelukast with or without levocetirizine or placebo; arm B, 20 patients received desloratadine, montelukast with or without desloratadine or placebo. All treatment periods lasted 6 weeks and were separated by 2-week washouts. At baseline and on the last day of each treatment period, SPT were performed in all participants.

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The bilateral hemispheric ischemia in rats was induced by the occlusion of bilateral common carotid arteries after permanent electrocauterization of bilateral vertebral arteries at the level of the second cervical vertebra. In ischemic rats, (a) electroencephalograms became flat immediately after occlusion of carotid arteries, and (b) mortalities reached maximum levels at day 3 after recirculation. These results suggested that a constant level of cerebral ischemia was produced in this rat model. Pentobarbital markedly inhibited the mortality in these ischemic rats, whereas cyproheptadine did not.

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The present study was designed to examine the possible involvement of both an anti-serotonin action and a catecholamine-stimulating action in the mechanism of the inhibition of the muricide in rats with lesions of the midbrain raphe. Serotonin antagonists, such as cyproheptadine (10 mg/kg), cinanserin (10 mg/kg) and pirenperone (1 mg/kg), given alone showed little suppression of muricide in rats with raphe lesions, although the first two drugs were inhibitory at very large doses. Methamphetamine showed no inhibition of muricide at 0.32 mg/kg (i.p.), but exerted a marked inhibition of muricide when combined with the above serotonin antagonists. In addition, the dose-response curve for cyproheptadine and cinanserin was shifted markedly to the left when combined with L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS) (100 mg/kg i.p.), but not with lisuride (0.32 mg/kg i.p.). Similarly, pirenperone produced a marked inhibition of muricide at doses of 0.32-1.8 mg/kg (i.p.) when combined with L-threo-DOPS, but not when combined with lisuride. These results suggest that the combination of an anti-serotonin action with noradrenergic activation is important for inhibiting muricide, at least in rats with raphe lesions. A similar mechanism also seems to be valid for the anti-muricidal effect of antidepressant drugs.

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Structural elucidation is an integral part of drug discovery and development. In recent years, due to acceleration of the drug discovery and development process, there is a significant need for highly efficient methodologies for structural elucidation. In this work, we devised and standardized a simple and economical online hydrogen-deuterium exchange methodology, which can be used for structure elucidation purposes. Deuterium oxide (D2O) was infused as a postcolumn addition using the syringe pump at the time of elution of the analyte. The obtained hydrogen/deuterium (H/D) exchange spectrum of the unknown analyte was compared with the nonexchanged spectrum, and the extent of deuterium incorporation was delineated by using an algorithm to deconvolute partial H/D exchange, which confirmed the number of labile hydrogen(s) in the analyte. The procedure was standardized by optimizing flow rates of LC output, D2O infusion, sheath gas, and auxiliary gas using the model compound sulfasalazine. The robustness of the methodology was demonstrated by performing sensitivity analysis of various parameters such as concentrations of analyte, effect of matrices, concentrations of aqueous mobile phase, and types of LC modifiers. The optimized technique was also applied to chemically diverse analytes and tested on various mass spectrometers. Moreover, utility of the technique was demonstrated in the areas of impurity profiling and metabolite identification, taking pravastatin-lactone and N-oxide desloratidine, as examples.

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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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The mechanism of action of 5-hydroxytryptophan (5-HT, 10 mg/kg), quipazin (7 mg/kg), zimelidin (15 mg/kg) and m-chlorophenylpiperazine (5 mg/kg) was examined with the aid of some analyzer substances. The avoidance behavior under stress was used as criterion of estimation. The optimizing effect of 5-HT on the avoidance behavior was demonstrated to be a consequence of serotonin synthesis activation and its release with activation of postsynaptic 5-HT-1-receptors. An adverse effect of quipazin on the avoidance behavior was, to a greater degree, due to the activation of 5-HT-2-autoreceptors rather than of dopamine receptors. The inhibitory effect of m- chlorphenylpiperazine was reversed by administration of pyrenepyrone , a blocker of 5-HT-2-receptors. The inhibitory effect of zimelidine on the avoidance behavior was not removed by clonidin . The positive effect on the avoidance behavior under stress occurs as a result of exposures that activate the synthesis and release of 5-HT as well as of activation of postsynaptic 5-HT-1 receptors.

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We characterized the serotonin (5-hydroxytryptamine; 5-HT) receptor mediating cilia-driven rotational movement in embryos of the freshwater gastropod Physa elliptica. In addition, putative serotonin reuptake inhibitors (SSRIs), previously shown to induce other 5-HT-mediated processes in molluscs, were tested for their ability to induce rotation. As in previous studies with other freshwater gastropods, 5-HT induced a significant dose-dependent increase in rotation from 10(-6) to 10(-4) M. The 5-HT(1A) agonist 8-OH-DPAT produced a similar dose-dependent increase in rotation. However, the 5-HT(2) agonist alpha-CH3-serotonin evoked a significant rotational response only at the highest concentration of 10(-4) M. The 5-HT(2) receptor antagonist mianserin not only blocked 5-HT-induced rotation, it reduced rotation rate below that of baseline. However, two other antagonists, cyproheptadine (5-HT(2)) and propranolol (5-HT(1)), caused similar responses that consisted of an initial rotational surge followed by reduced rotation. Thus, these drugs appear to act as partial agonists. The putative SSRI fluvoxamine exhibited a significant dose-dependent increase in positive rotation as that seen with 5-HT. The SSRIs paroxetine and fluoxetine both caused an increase in rotation at 10(-6) and 10(-5) M but reduced rotation rate below that of baseline at 10(-4) M. These results agree with other studies on aquatic molluscs, suggest a 5-HT receptor with a mixed 5-HT(1)/5-HT(2) pharmacological profile and add to a now growing body of literature on the pharmacology of molluscan 5-HT receptors. In addition, all the tested putative SSRIs induced cilia-driven rotation in Physa embryos, indicating either the presence of 5-HT reuptake transporters or that these compounds act as 5-HT receptor ligands. J. Exp. Zool. 286:414-421, 2000.

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buy periactin generic 2016-05-07

Tail thrombosis (infarction) induced by injection of kappa-carrageenin (0.88 or 1.76 mg/ periactin buy kg i.v.) is increased by i.v. or i.p. serotonin (1-2 mg/kg) but is decreased by cyproheptadine and ketanserin (minimal effective dose less than 1 mg/kg) as well as by preceding serotonin depletion by comp. 48/80 or reserpine. The effect of exogenous serotonin is antagonized by ketanserin and cyproheptadine, respect. In the anaphylactoid reaction induced by dextran, only weak thrombosis increasing effects were seen, apparently, because of vasodilation in this reaction. Application of heat to the tail weakly decreased tail thrombosis, application of cold strikingly increased it. Vasodilating substances (nicotinate, 3-hydroxymethylpyridine, trapidil, dipyridamole, iloprost) as well as the thromboxane antagonist BM 13,177 were without significant effect on tail thrombosis, even if vasodilating substances were applicated in form of ointments on the tail. The participation of endogenous serotonin in carrageenin-induced tail thrombosis has further to be substantiated.

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Several 5-HT uptake inhibitors, established and potential antidepressant drugs, were tested for their ability to counteract contractions of the rat isolated stomach fundus strip induced by 5-HT and BaCl2. Of 12 inhibitors tested, only doxepine, amitriptyline, clomipramine, imipramine, Ro 11-2465 (cyan-imipramine), citalopram and fluvoxamine antagonized the contraction induced by 10(-6) M 5-HT with IC50 values below 10(-4) M. Amitriptyline, doxepine and cyproheptadine, at concentrations inhibiting the effect of 5-HT, did not antagonize the strip contractions induced by 3 X 10(-3) M BaCl2, while the remaining compounds that antagonized 5-HT-induced contractions, also antagonized--with at periactin buy least a similar potency--the contractions induced by BaCl2. From among antidepressant compounds investigated, only doxepine and amitriptyline may be regarded as antagonists of the 5-HT receptor in the rat stomach strip.

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Of the 58 chambers (47 patients), which were all strongly positive (+ +) during the 1st patch test, the situation was unchanged in 51 chambers Voltaren Dosage 50mg ; 4 + reactions and 2 + + + reactions were observed; and 1 chamber was negative. There was no statistically significant difference when comparing the scores of the 1st assessment with those of the 2nd (p = 0.206). If the patch test reaction of the patient who dropped out of the trial had changed from strongly positive (+ +) to negative, there would still have been no statistically significant difference between the score of the 1st assessment with those of the 2nd ( p = 0.107).

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The effect of a series of indoleamines on the potassium-evoked release of previously accumulated [3H]serotonin from slices of rat raphe nuclei has been studied. Indoleamine agonists produced a dose-related inhibition of potassium-evoked tritium release which was reversed by Aciphex Dosage methiothepin, metergoline, mianserin and methysergide but not cyproheptadine or cinanserin. The relative order of antagonist potency for this effect was different from that obtained for the antagonism of indoleamine-induced inhibition of potassium-evoked tritium release from rat striatal slices previously loaded with [3H]-dopamine. The results show that the serotonin-autoreceptor located on cell bodies and dendrites in the raphe nucleus is different from the postsynaptic serotonin receptor located on dopamine nerve terminals in the striatum.

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Department of Physiology, Indocin Capsule University of Zimbabwe.

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eNOS might play a more important role than Buy Strattera Online iNOS in regulating the NO level of the nasal tissue of the guinea pigs suffered from allergic rhinitis, and desloratadine had no involvement in regulating the expression of iNOS and eNOS.

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By gel filtration on a Fractogel TSK HW 50 column followed by cation-exchange chromatography on CM-Trisacryl M, a tetradecapeptide amide, designated 'mastoparan B', was purified from the venom of the hornet Vespa basalis. Its amino acid sequence was determined as: Leu-Lys-Leu-Lys-Ser-Ile-Val-Ser-Trp-Ala-Lys- Zanaflex Tizanidine Reviews Lys-Val-Leu-NH2 and its molecular mass was measured to be 1611 Da by fast-atom-bombardment mass spectrometry. In addition to having a common structure of vespid mastoparans, the peptide shows a less hydrophobic sequence at positions 1, 2, 5, 8 and 9. The peptide caused liberation of histamine from rat peritoneal mast cells and induced oedema in the rat paw. However, the latter effect was inhibited by 'anti-serotonin' (anti-5-hydroxytryptamine) (cyproheptadine), but not by antihistamine (chlorpheniramine). The peptide also possesses a potent haemolytic activity which acts in synergy with the lethal protein of the venom, suggesting the possible involvement of mastoparan B in the lethal effect of Vespa basalis venom.

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In a double-blind, crossover, randomized clinical pharmacological study performed on 10 healthy volunteers, peripheral and central effects of 10 mg cetirizine and 10 and 40 mg loratadine were compared. Cetirizine (10 mg) significantly (P less than 0.001) inhibited 10 or 100 mg/ml histamine-induced weals 2 and 6 h after drug intake. Cetirizine was more potent than 10 mg loratadine after 2 and 6 h, and was Elavil 5 Mg even more potent than 40 mg loratadine after 6 h. Neither drug affected subjective evaluation of central effects and cetirizine was completely devoid of electro-encephalographic (EEG) changes, whereas 10 and 40 mg loratadine induced only slight and limited EEG changes.

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Present results showed that single oral doses of rupatadine Glucotrol Diabetic Pills 10 mg in combination with alcohol do not produce more cognitive and psychomotor impairment than alcohol alone. Higher doses of rupatadine, in combination with alcohol, may induce cognitive and psychomotor deterioration as hydroxyzine and cetirizine at therapeutic doses.

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Cognitive impairment in schizophrenia patients is associated with poor outcome and it represents one of main challenges of pharmacological treatment. Unfortunately, second-generation antipsychotics have not yielded the expected results in the improvement Sporanox Online Pharmacy of these symptoms.

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The effects of 5-HT agonists and antagonists, benzodiazepine anxiolytics and tricyclic antidepressants on restraint stress-induced anorexia in rats were examined. The selective 5-HT(1A) agonists 8-hydroxy-2-(di- n-propylamino)tetralin (8-OH-DPAT), buspirone and ipsapirone, when injected 2 h after the termination of stress, attenuated stress-induced anor exia and body weight loss. The effects of 8-OH-DPAT on stress-induced anorexia were blocked by the 5-HT(1A) antagonist spiperone but not by the 5-HT(2) antagonist ketanserin. The preferential 5-HT(1B) agonists RU-24969 and quipazine induced anorexia in unstressed rats and tended to supplement the anorectic effects of stress. The benzodiazepines chlordiazepoxide and diazepam and the 5-HT antagonist cyproheptadine had no effect on stress-induced anorexia Cymbalta Substitute Generic , when given (like the 5-HT(1A) agonists) 2 h after the stress. Similarly, daily injection for 2 weeks of the tricyclic antidepressants desipramine and sertraline had no beneficial effect. The data suggest that 8-OH-DPAT, buspirone and ipsapirone attenuate stress-induced anorexia in rodents by a hyperphagic action on 5-HT(1A) receptors.

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This randomized, double-blind, crossover study compared the effects of the R-enantiomer of cetirizine, levocetirizine, with those of loratadine on the wheal, flare, and itch response to histamine in human skin.

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Thus, our results do not support previous observations that serotonin metabolism itself is a major factor behind anorexia in tumor-bearing animals in general. Rather, other mechanisms, such as eicosanoid and nitric oxide-dependent pathways, seem to be more important for induction of anorexia along tumor progression in the present model.

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A simple, rapid, and sensitive visible spectrophotometric method was developed, for the first time, for analysis of desloratadine (DE) in tablets. The method is based on the deep-blue colored TCNQ*- radical anion formed by interaction of the drug (n-donor) with 7,7,8,8-tetracyanoquinodimethane (TCNQ, pi-acceptor) in acetonitrile at ambient temperature. Optimum conditions for the reaction were investigated, absorbances were read at 843 nm, and the linearity range for concentrations of DE was found to be 1.5-13 microg/mL. The reaction product remains stable up to 8 h when kept at room temperature in the dark. The developed method was validated and successfully applied to the determination of DE in tablets. The tablets were also analyzed with a column liquid chromatography method reported in literature. The results from both methods were statistically compared by t- and F-tests. No significant difference was found for the means and standard deviations at 95% confidence level. Accuracy was examined through recovery studies. Being very simple and reliable, the method can be recommended for routine quality control analysis of DE in tablets.