Drugs online research references
Gastroenterology. 1996 Jan;110(1):121-8.
Mast cells mediate acid-induced augmentation of opossum esophageal blood flow via histamine and nitric oxide.
Feldman MJ, Morris GP, Dinda PK, Paterson WG.
Gastrointestinal Diseases Research Unit, Hotel Dieu Hospital, Kingston, Ontario, Canada.
BACKGROUND & AIMS: Increased esophageal blood flow during reflux episodes may play an important role in mucosal resistance to injury, although the mechanism remains unclear. Decreased stainable mast cells and increased luminal histamine release during acid exposure has been previously documented. Therefore, the role of mast cells, nerves, histamine, and nitric oxide in mediating increased blood flow during acid challenge of the distal esophagus was investigated. METHODS: The effects of the mast cell stabilizers disodium cromoglycate and doxantrazole, the neurotoxin tetrodotoxin, the histamine H1 receptor antagonist promethazine, and the NO synthase inhibitor N omega-nitro-L-arginine methyl ester were examined by monitoring opossum esophageal histamine release and blood flow during perfusion with 100 mmol/L HCl. RESULTS: Luminal acid challenge significantly increased both histamine release and blood flow (P < 0.05). Disodium cromoglycate, promethazine, and N omega-nitro-L-arginine methyl ester attenuated the increase in blood flow to basal (saline-perfused) levels. Tetrodotoxin did not prevent an acute increase in blood flow that rapidly returned to baseline, likely from the ensuing hypotension. CONCLUSIONS: These findings provide evidence that mast cell-derived histamine, acting through an NO-dependent mechanism, plays a central role in the response of the esophageal microcirculation to luminal acid.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8536848&dopt=Abstract
Acta Microbiol Immunol Hung. 1995;42(3):277-85.
Interaction between tricyclic psychopharmacons and some antibiotics.
Molnar J, Batho N, Csik V, Chevalier J, Cremieux A.
Institute of Microbiology, Albert Szent-Gyorgyi University Medical School, Szeged, Hungary.
The tricyclic psychopharmacons, e.g. clozapine, promethazine and imipramine cure plasmids and inhibit plasmid transfer among bacteria due to the inhibition of supercoiling activity on DNA gyrase. In addition an interaction was found between clozapine, imipramine, promethazine and some antibiotics, e.g. penicillins and tetracycline in vitro. The nature of interaction is based on a charge transfer complex, which is formed between clozapine, imipramine, promethazine and penicillins. Differential spectrophotometry showed that ampicillin reduced the highest energy peaks of clozapine, promethazine and imipramine. Streptomycin did not alter the spectrum of clozapine; however, tetracycline somewhat reduced all the peaks of clozapine. Clozapine and promethazine exhibited a synergistic effect with ampicillin, tetracycline and gentamicin on Escherichia coli cells in in vitro. This kind of interaction was missing in the case of imipramine.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8548201&dopt=Abstract
Clin Exp Allergy. 1995 Oct;25(10):974-84.
Antihistamine activity, central nervous system and cardiovascular profiles of histamine H1 antagonists: comparative studies with loratadine, terfenadine and sedating antihistamines in guinea-pigs.
Hey JA, Del Prado M, Cuss FM, Egan RW, Sherwood J, Lin CC, Kreutner W.
Schering-Plough Research Institute, Kenilworth, NJ, USA.
BACKGROUND: Sedation limits the clinical utility of classical H1 antihistamines, while newer antihistamines such as loratadine and terfenadine are non-sedating. However, clinical use of the terfenadine has been associated with rare but severe cardiac arrhythmias, in particular torsades de pointes. OBJECTIVE: To establish a quantitative experimental model for assessing the sedating and cardiotoxicity potential of non-sedating and sedating antihistamines. METHODS: Drugs were administered intravenously and the integrated amplitude of the cortical electroencephalogram (EEG) signal was recorded. The threshold dose that depressed EEG activity was compared with the dose required to inhibit by 50% the peripheral bronchospasm elicited by 10 micrograms/kg i.v., of histamine. In separate studies, the electrocardiogram (ECG) and cardiovascular effects of loratadine (30 and 100 mg/kg, i.v.), terfenadine (10 mg/kg, i.v.), promethazine (5 mg/kg, i.v.) and diphenhydramine (20 mg/kg, i.v.) were evaluated. RESULTS: The sedating antihistamines, diphenhydramine and promethazine, depressed the integrated EEG at doses between 0.6 and 2.0 times their peripheral antihistamine doses. Loratadine had no EEG depressant activity at 100 mg/kg, i.v., a dose more than 170 times its ED50 (0.58 mg/kg, i.v.) against histamine bronchospasm. We were unable to evaluate the EEG effects of terfenadine, because it produced cardiovascular collapse at 10 mg/kg, i.v. Loratadine and promethazine did not produce adverse cardiovascular effects, nor did they alter normal ECG activity. Diphenhydramine produced bradycardia followed by a transient hypertensive phase without affecting the QTc interval. In contrast, terfenadine elicited hypotension, bradycardia and significant arrhythmogenic activity, causing a prolongation of the QTc interval and a torsades de pointes--like ventricular arrhythmia. Pharmacokinetic studies after i.v. administration of loratadine (30 and 100 mg/kg) demonstrated plasma levels of loratadine and its major metabolite descarboethoxyloratadine to be several orders of magnitude greater than levels found in humans at the clinical dose of 10 mg. CONCLUSION: The CNS depressant effects of H1 antihistamines are promethazine approximately diphenhydramine >> loratadine = placebo. Of the non-sedating antihistamines, loratadine was devoid of adverse cardiovascular effects whereas terfenadine caused a pronounced disruption of the normal ECG, characterized by a torsades de pointes-like effect.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8556569&dopt=Abstract
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