The development of bronchospasm is shown to be accompanied by hpid peroxidation (LPO) activation; 3-fold and 8-fold rises of malondialdehyde concentration are found in homogenate of lung from sensitized animals and from animals provoked with egg albumin antigen, respectively. The use of luminol-dependent chemiluminescence (CL) reveals that in sensitized rats the production of oxygen free radicals is increased by alveolar macrophages activated with phorbol myristate acetate. Troventol at 10 -3 mg/rnl inhibits the CL response of phagocytes both in intact and in sensitized rats and lowers the level of Fe2+-induced LPO in lung tissue but not in the liver of intact animals.
Donnan potential recordings demonstrate that the preparation troventol exhibits a positive surface charge, atropine sulfate a negative surface charge, and atrovent a charge close to zero. Analysis of electrostatic interactions between these preparations and cells reveals that alveolar macrophages exhibit a more negative surface charge than peritoneal macrophages. More pronounced electrostatic interactions of the preparations with membrane macrophages are observed with troventol versus the other broncholytics studied.
Molecular mechanism of the effect of the anticholinergic bronchodilator troventol on histamine secretion, the initial step in bronchospasm, is studied. Atrovent (ipratropium bromide) and atropine sulfate are used as reference preparations. Histamine secretion is induced by adding phorbol myristate acetate to cell suspension. In cells incubated for 5 rain with troventol histamine secretion constitutes 52.4% of the maximum level, while atrovent and atropine have no effect on this process. Histamine secretion in mast cells is initiated by a sharp increase in cytosolic calcium. Troventol and atrovent reduce the initial rate of passive calcium entry into the cells by 56.3 and 28%, respectively, while atropine does not affect this parameter.
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