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The present results suggest that rupatadine 10 mg a day may be a valuable and safe alternative for the symptomatic treatment of seasonal allergic rhinitis.
The drugs proposed are considered according to their site of action. Synthetic anti-cortisol drugs (Op'DDD in particular and aminoglutethimide) appear to be the drugs of choice at present. They act on the adrenals, but research is now being carried out on drugs which act on ACTH secretion, E.g; cyproheptadine and bromocriptine.
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A 9-month-old female Labrador retriever was evaluated after ingestion of a 5-HTP supplement. Signs of agitation developed within 1 h of ingestion, and emesis was attempted by the owner with 3% hydrogen peroxide (H2O2) orally. On presentation, the dog was obtunded, bilaterally mydriatic and salivating. Physical exam revealed tachypnea, tachycardia, hyperthermia, and hypertension. Eighteen hours post presentation, the dog developed melena, hematemesis, and pigmenturia. A hemogram revealed mild anemia with evidence of oxidative erythrocyte damage (eccentrocytes, Heinz bodies, and siderocytes). A chemistry panel revealed markedly elevated creatine kinase and hyperbilirubinemia, supporting hemolytic anemia. A urinalysis revealed pigmenturia. Hemolytic anemia was presumed to be caused by oxidative damage secondary to gastrointestinal ulceration and circulatory embolism of H2O2. Treatment included fluid therapy, a mannitol constant rate infusion, antiemetics, gastroprotectants, and cyproheptadine as a serotonin antagonist. The patient responded well to treatment and was discharged within 48 h of presentation.
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BALB/c mice were systemically sensitized with ovalbumin (OVA) (six times, days 1-14) and challenged with aerosolized allergen (days 28-30). One day prior to the first and 2 h prior to every following sensitization, mice received either 1 or 0.01 microg of desloratadine (DL) or placebo per os.
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1 The intravenous injection of pethidine in rabbits pretreated with furazolidone administered orally but not systemically resulted in severe interaction and fatal hyperpyrexia. 2 Treatment with rho-chlorophenylalanine, chloropromazine of cyproheptadine protected the rabbits against the furazolidone-pethidine interaction, while alpha-methyl-rho-tyrosine was ineffective. 3 5-Hydroxytryptophan produced a fatal hyperpyrexia in furazolidone pretreated rabbits. 4 Pretreatment of rabbits with 1,1,1-trichloro-2, 2-bis(rho-chlorophenyl)ethane (DDT) accelerated and enhanced the furazolidone-pethidine interaction, while oxytetracycline pretreatment completely prevented the interaction. 5 It is concluded that furazolidone-pethidine interaction might depend mainly on potentiation of the effects of 5-hydroxytryptamine in the CNS and that the transformation of furazolidone into an active monoamine oxidase inhibitor metabolite might occur mainly in the gut microflora in the gut lumen.
Pituitary adenomas may produce local endocrine and neurological effects, as well as systemic metabolic complications due to hormonal hypersecretion. Medical therapy with pharmacological agents has been developed and is based on the neurotransmitter regulation of normal pituitary hormonal secretion. 189 patients with secretory pituitary adenomas underwent medical therapy for the hypersecretory state. 156 of these were prolactin-secreting adenomas, 16 of which were in males. The response of bromocriptine was almost universal with lowering of serum prolactin and reversal of the clinical symptoms, as well as tumor shrinkage of most large adenomas with suprasellar extension. 23 patients with acromegaly were treated with bromocriptine, with 11 noting clinical improvement, and decreased tumor size in two. Five patients with Cushing's disease were treated with cyproheptadine, with only one showing a biochemical and clinical improvement. Two patients with Nelson's syndrome each had progressive tumor growth stabilized with cyproheptadine and bromocriptine in one, and sodium valproate in the other. There appears to be a role for medical therapy in the majority of prolactin-secreting pituitary tumors, some growth hormone secreting pituitary tumors, and selected adrenocorticotropin secreting-pituitary tumors.
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Less than Glu-His-Pro-OH or 'acid' TRH, until now considered to be an inactive metabolite of TRH, induces in rats when administered intracerebroventricularly (i.c.v.), stereotyped behavior and, from 12.5 micrograms, wet-dog shakes (WDS). WDS induced by 200 micrograms less than Glu-His-Pro-OH are antagonized by apomorphine, haloperidol and cyproheptadine while phentolamine and naloxone are without effect. For this action 'acid' TRH appears as effective as TRH itself and might have the same mechanism.
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Various drugs acting on brain serotonin or catecholamines were administered concurrently with morphine during the development of dependence or before naloxone-precipitated withdrawal syndrome. Of the various drugs only cyproheptadine, a serotonin antagonist, and piribedil, a dopamine agonist, reduced the frequency of jumping (but not of diarrhea or ptosis) when administered with morphine during development of dependence. When administered before naloxone, d-fenfluramine, a serotonin releaser, markedly reduced jumping, but not diarrhea and ptosis, and clonidine blocked these latter signs without affecting the frequency of jumping. Of the other drugs examined only phenoxybenzamine reduced diarrhea in morphine-abstinent rats. It is suggested that serotonin is involved in the mechanisms which lead to compulsive jumping during naloxone-precipitated withdrawal, whereas adrenergic sites on which clonidine acts are mainly involved in the expression of signs, such as ptosis and diarrhea. No clear evidence was obtained of a role for dopamine in the withdrawal signs studied.
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Head-twitches have been regarded as an experimental model of hallucination, and we have recently observed that p-hydroxyamphetamine (p-OHA) markedly induced head-twitches in mice. The present work was undertaken to study possible participation of a serotonergic system in the mechanism of head-twitches induced by p-OHA. Head-twitches induced by p-OHA continued for 20-80 min, and the peak time of this effect was approximately 30-40 min after the administration. The i.c.v. administration of p-OHA (20, 40, 80 and 160 micrograms/mouse) produced characteristic head-twitches in a dose-dependent manner. Simultaneous injection of serotonin (10 micrograms/mouse, i.c.v.) and p-OHA caused a 2-2.5-fold increase in the number of head-twitches compared with non-serotonin controls. Pretreatment with p-chlorophenylalanine (200 mg/kg, i.p. and 500 micrograms/mouse, i.c.v.), in contrast, reduced head-twitches as did the pretreatment with cyproheptadine or dimethothiazine. These results suggest that p-OHA-induced head-twitches may involve the central serotonergic system which may exert an excitatory effect on head-twitches.
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Arachidonic Acid (AA) injected into a hindpaw of Lewis rats produces high levels of tissue myeloperoxidase (MPO), a biochemical marker for PMN leukocytes. Treatment with a corticosteroid (prednisolone) or dual 5-LO/CO inhibitors of AA metabolism (phenidone, SKF 86002) produced dose-related inhibition of AA-induced elevations in paw tissue MPO levels. In contrast, administration of high pharmacologic doses of selective cyclooxygenase inhibitors (indomethacin, ibuprofen, naproxen), anti-histamine/serotonin agents (cyproheptadine, chlorpheniramine) or an anti-arthritic gold compound (auranofin) produced only slight or moderate effects. Thus, AA-induced hindpaw inflammation is a useful method for determining pharmacologic effects of 5-LO/CO inhibitors on PMN leukocyte infiltration in vivo.
Neurotransmitters and neuropeptides interact in several ways. We studied a new type of interaction: the effect of neurotransmitters on the saturable system that transports Tyr-MIF-1 and the enkephalins out of the central nervous system (CNS). The neurotransmitters were introduced into the lateral ventricle of the brain with radioiodinated peptide, using an established method previously shown to accurately quantify the amount of peptide being transported from the CNS to the blood. Serotonin inhibited transport, histamine stimulated transport, and dopamine, acetylcholine, epinephrine, GABA, kainic acid, cAMP and cGMP were without effect. Cyproheptadine, a serotonin antagonist, stimulated transport. Of several psychotropic agents tested, only tranylcypromine had a statistically significant effect and stimulated transport. Of the serotonin receptor specific agents tested, those with 5HT1 activity most consistently affected transport. We conclude that serotonin, and perhaps histamine, are important modulators of the system that transports Tyr-MIF-1 and the enkephalins out of the CNS.
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Biological activities of C3 beta c, which is a C-terminal fragment of the beta-chain of rat complement C3, have been studied by in vivo and in vitro experiments. C3 beta c was purified as a novel neutrophil chemoattractant from the exudate of the chronic phase of rat carrageenin-induced inflammation. The purified C3 beta c induced neutrophil chemotaxis in vivo when C3 beta c was injected into the preformed air-pouch on the back of rats. C3 beta c transiently increased the intracellular free Ca2+ concentration of neutrophils and enhanced the adhesion of neutrophils to fibrinogen in vitro, suggesting that C3 beta c has the ability to express an adhesion molecule of rat neutrophils. In addition, C3 beta c at low concentrations (10(-10)-10(-11) M) stimulated rat macrophages to produce cytokine-induced neutrophil chemoattractant-2, a member of the interleukin-8 family. Furthermore, C3 beta c enhanced vascular permeability in vivo, which is suppressed by cyproheptadine, suggesting that C3 beta c may have the characteristics of an anaphylatoxin. Our results suggest that C3 beta c contributes to oedema formation and neutrophil accumulation at inflammatory sites in rats.
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Both groups showed improvements in exercise parameters after loratidine therapy compared to basal EST results. ST(max) ( group A: 1.9 +/- 0.74 vs 0.9 +/- 1.29 mm, P = .046; group B: 2.5 +/- 0.71 vs 1.4 +/- 1.17 mm, P = .041), ST(lead) ( group A: 3.4 +/- 1.08 vs 1.5 +/- 2.12, P = .027; group B: 4.6 +/- 1.71 vs 2.22 +/- 2.25, P = .011), ST(total) ( group A: 4.7 +/- 2.18 vs 2.1 +/- 3.11 mm, P = .024; group B: 7.9 +/- 2.92 vs 3.33 +/- 3.81 mm, P = .005).
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Levocetirizine (5 mg), loratadine (10 mg), or placebo was taken orally 4 h before the intradermal injection of histamine (20 microl, 100 microM) or the control vehicle into the forearm skin of healthy volunteers. Flare areas were assessed by scanning laser Doppler imaging before and at 30-s intervals for a period of 9 min. Wheal areas were measured by planimetry at 10 min. Itch was scored every 30 s with a visual analogue scale.
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Gas-liquid chromatographic and mass, nuclear magnetic resonance, and infrared spectrometric techniques were utilized to identify some of the metabolites of cyproheptadine in the urine of human subjects who had ingested radiolabeled drug. Aromatic ring hydroxylation (followed by glucuronide conjugation), N-demethylation, and heterocyclic ring oxidation were shown to occur in man. The principal metabolite, however, was identified tentatively as a quaternary ammonium, glucuronide-like conjugate of cyproheptadine. No evidence was found for metabolic changes at the tricyclic ethylene bridge in this species.
The basophil activation test (BAT) is a widely validated and reliable tool especially for the diagnosis of hymenoptera venom allergy. Nevertheless, several pitfalls have to be considered and outcomes may differ because of diverse in-house protocols and commercially available kits. We aimed to identify the factors that may influence results of the CD63-based BAT.
Eighteen healthy young subjects of both sexes took part in a crossover, randomised, double-blind, placebo-controlled study. Treatments tested were: RU 10, 20, 40 and 80 mg and hydroxyzine 25 mg, as a positive standard. Before and several times after drug intake, peripheral anti-H1 activity was appraised by the skin reactivity to intradermal injection of histamine. CNS effects were also obtained by objective tests of psychomotor performance and subjective mood scales.
1. The inflammatory response induced by poly-L-arginine in the rat hind-paw was studied both by measuring paw oedema and histologically. 2. The paw volume was measured with a hydroplethysmometer at 0.5, 1, 2, 4, 6 and 18 h after the subplantar injection of the polycation. Protein extravasation was evaluated with Evans' blue and the histology studied by light microscopy. 3. Poly-L-arginine (12, 24, 43 and 115kD) caused dose- and molecular weight-dependent oedema which had a rapid onset and long duration. Evans' blue extravasation paralleled the oedema induced by poly-L-arginine. Microscopic examination of the paws at early stages of oedema formation showed exuberant liquid exudate with no inflammatory cells. After 18 h, a cellular infiltrate was present, consisting mainly of mononuclear cells. 4. Indomethacin, dexamethasone, BW755c or the PAF-antagonist WEB 2086 caused no significant inhibition of the poly-L-arginine-induced oedema. Cyproheptadine had inhibitory effects only on the early stages of the polycation-induced oedema. Similar results were observed with rats depleted of histamine and 5-hydroxytryptamine. 5. Heparin, a polyanion, injected in the rat paw caused a marked inhibition of the polycation-induced oedema. NG-monomethyl-L-arginine (LNMMA), an inhibitor of EDRF synthesis, injected locally also produced a marked inhibition, but this inhibition was reversed by iloprost. 6. These results suggest that the oedema induced by polycations was due to their cationic charge. The inhibitory effect of LNMMA is probably due to a decrease in vascular flow rather than a decrease in vascular permeability.
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Desloratadine 5 mg once daily was associated with significant improvement in symptoms of SAR, and appeared to provide additional benefit in relieving moderate to severe nasal stuffiness/congestion in 6786 patients receiving 7-day treatment in an actual practice setting of primary care physicians in Canada.
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Cytotoxic properties of plant extracts and drugs being developed for cancer treatment are usually evaluated by a variety of in vivo and in vitro tests carried out in animal or plant based models. In the present study we have evaluated the possibility of using the germinating mung beans (Vigna radiata), for rapid and inexpensive screening of drugs exhibiting cytotoxic properties. Mung beans were allowed to germinate either in tap water or in different drug solutions, and parameters like percent germination, increase in radicle length, change in seedling weight and mitotic index of apical root meristems were determined at two time intervals coinciding with the time at which the radicle length in control group was 1.0 to 1.5 cm (time 0, T0) and 48 h later (T48). Methanol extract of Calotropis procera latex as well as drugs like podophyllotoxin, cyclophosphamide, cyproheptadine and aspirin produced a dose-dependent inhibitory effect on seed germination, seed weight gain, radicle growth and mitotic index in the radicle meristems. The inhibitory effect of some of the drugs tested was associated with reduction in water imbibition. Some of the drugs at higher concentrations allowed seed germination to take place but produced radicle decay and seedling weight loss. Our study shows that germinating V radiata beans could be used as a convenient model for the preliminary screening of drugs exhibiting cytotoxic properties.
It was concluded that four common treatment modalities could effectively release symptom scores, but decrease of airway inflammation as determined by decrease of eNO might be only achieved by nasal budesonide and montelukast, but not nasal sodium cromoglycate and loratadine. Children with perennial allergic rhinitis with high eNO levels may require oral montelukast or nasal budesonide treatment to prevent airway hyperresponsiveness.
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There was no significant overall diurnal variation of basophil numbers in healthy controls or chronic urticaria patients. Mean (SE) manually counted basophil were higher in healthy controls than chronic urticaria (43.4/ microL (2.1) vs. 4.4 (0.8), P < 0.001). Basophil counts were reduced in healthy controls on steroids (19.2 (1.9), P < 0.001) but increased in chronic urticaria (8.9 (1.9), P < 0.001). Loratadine did not influence them. UAS fell on treatment (3.3 (0.4) baseline, 1.4 (0.5) on loratadine and 0.5 (0.2) on prednisolone with loratadine, P < 0.001). There was a negative linear correlation between basophil numbers and UAS in untreated chronic urticaria patients (P = 0.001, Spearman rank correlation). Manual and automated basophil counts showed poor agreement. Lymphocyte numbers were lower in chronic urticaria than healthy controls. Neutrophils increased whereas lymphocytes and eosinophils decreased in all subjects on prednisolone. They were unaffected by loratadine.