Springer Online Journal Archives 1860-2000
Abstract At a concentration of 1×10−4 M (28.84 Μg/ml), with a solvent concentration of 1.0% (v/v) ethanol, the deacetylated (amine) metabolite of diamphenethide (DAMD) causes an initial stimulation of activity, followed by suppression, leading to a paralysis within 3 h. These changes are accompanied by an increase in muscle tone of more than 200 mg. However, ethanol alone at a concentration of 1.0% (v/v) causes an initial stimulation of activity and increase in muscle tone (approximately 550 mg). If the concentration of DAMD is kept at 1×10−4 M (28.84 Μg/ml) but the solvent concentration reduced [e.g., 0.05% (v/ v) dimethyl sulphoxide], then only a suppression of motility and flaccid paralysis are observed. This response is also seen at the lower concentration of 10 Μg/ml, which corresponds to the maximum blood levels of DAMD in vivo. The sodium ionophore monensin induces a suppression of motility, leading to a rapid flaccid paralysis (in approximately 1.5 h at 1×10−7 M, and within a few minutes at higher concentrations). Ouabain, an inhibitor of Na+/K+-ATPase activity, also causes a suppression of motility, but this is accompanied by an increase in muscle tone, leading to a spastic paralysis (in approximately 2.5 h at 1×10−3 M, and 3.5 h at 1×10−4 M). Pretreatment with ouabain (1×10−3 M for 15 min) followed by monensin (1×10−5 M) reverses the original effect of monensin by inducing a rapid spastic paralysis (in approximately 50 min). A similar effect is observed with DAMD (10 Μg/ml) following ouabain pretreatment; a spastic paralysis is reached after approximately 80 min. The results are discussed in relation to the postulated activity of DAMD as a sodium ionophore, Na+/K+-ATPase inhibitor, or neuromuscular depressant.
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