1 Neostigmine and BW284C51 induced concentration-dependent contractions in human isolated bronchial preparations whereas tetraisopropylpyrophosphoramide (iso-OMPA) was inactive on airway resting tone. 2 Neostigmine (0.1 pM) or iso-OMPA (100 pM) increased acetylcholine sensitivity in human isolated bronchial preparations but did not alter methacholine or carbachol concentration-effect curves. 3 In the presence of iso-OMPA (10 pM) the bronchial rings were more sensitive to neostigmine. The pD2 values were, control: 6.05 ± 0.15 and treated: 6.91 ± 0.14.4 Neostigmine or iso-OMPA retarded the degradation of acetylcholine when this substrate was exogenously added to human isolated airways. A marked reduction of acetylcholine degradation was observed in the presence of both inhibitors. Exogenous butyrylcholine degradation was prevented by iso-OMPA (1O pM) but not by neostigmine (O.1 pM). 5These results suggest the presence of butyrylcholinesterase activity in human bronchial muscle and this enzyme may co-regulate the degradation of acetylcholine in this tissue.

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ChemInform Abstract Coupling of camphor nitrimine (I) with the norbornenylmethylamine (II) yields the imine (III) which is reduced to give the amine (IV). This reacts with the isocyanates (V) or the aromatic acid chlorides (VII), producing the ureas (VI) or the carboxamides (VIII). The antiinflammatory, hypoglycemic, local anesthetic, antiarrhythmic, and hypotensive activities of the compounds (VI) and (VIII) are reported.

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The effects of teicoplanin on adenosine-diphosphate (ADP)-induced human platelet aggregation in vitro and on both ADP- and ristocetin-induced human platelet aggregation ex vivo were investigated. In the in vitro study carried out on platelets from 7 healthy volunteers, teicoplanin had no effect on platelet function even at a concentration (1 mg/ml) 10 times higher than the peak level found in the in vivo state, but at the highest concentration (10 mg/ml), which is 100 times higher than that reached in vivo, it inhibited ADP-induced platelet aggregation. In the ex vivo studies carried out in 10 healthy volunteers, teicoplanin, following single intravenous doses of 400 mg and 800 mg, did not produce any effect on platelet function up to 6 hours after administration. After 12 hours, teicoplanin, when given at 800 mg i.v., reduced ADP-induced platelet aggregation.