van den Brink F G, Offermeier J, Griessel H J
Scand J Respir Dis Suppl. 1977;98:47-50.
In certain cases beta-adrenergic substances cause little or no relaxation of tracheal or bronchiolar smooth muscles contracted by spasmogenic mediators. This phenomenon is explained on the basis of the model of functional antagonism, with the suppositions that the spasmogenic system has a reserve and the spasmogen concentrations are much higher than the concentration which would cause a just-maximal contraction. If this is correct, the model predicts that it should be possible to restore the effectiveness of the beta-adrenergic spasmolytics with low doses of a non-competitive (metactoid) spasmolytic, provided that this substance acts by depressing the subeffect curve. Such a metactoid antagonist should cause the desired result in subthreshold concentrations, i.e. concentrations which as such do not cause relaxation of the contracted muscles. In a series of experiments on the isolated tracheal chain of the guinea-pig the results agreed with this expectation. This provides additional proof for the model of functional interaction and suggests that the combination of beta-adrenergics with low doses of a metactoid spasmolytic may be of clinical interest.
在某些情况下，β-肾上腺素能物质对由致痉介质引起收缩的气管或细支气管平滑肌几乎没有或完全没有舒张作用。这种现象是根据功能拮抗模型来解释的，其假设是致痉系统有储备，且致痉原浓度远高于能引起最大收缩的浓度。如果这是正确的，该模型预测，只要一种非竞争性（类毒素）解痉剂通过压低副效应曲线起作用，那么用低剂量的这种解痉剂就应该有可能恢复β-肾上腺素能解痉剂的有效性。这样一种类毒素拮抗剂在阈下浓度，即本身不会引起收缩肌肉舒张的浓度下，应该能产生预期的效果。在一系列对豚鼠离体气管链的实验中，结果与这一预期相符。这为功能相互作用模型提供了额外的证据，并表明β-肾上腺素能药物与低剂量类毒素解痉剂的联合应用可能具有临床意义。
