Verrill H L, Pickard N A, Gruemer H D
Clin Chem. 1977 Dec;23(12):2219-25.
Above-normal plasma enzyme activities resulting from increased release of intracellular macromolecules are an important diagnostic feature of Duchenne muscular dystrophy. These and other biochemical and histological characteristics of this disease are faithfully duplicated when imipramine and serotonin are administered to the rat. Imipramine, but not serotonin alone, causes release of enzymes from rat diaphragms and human lymphocytes and release of hemoglobin from erythrocytes in vitro. Ouabain causes neither. Imipramine-induced enzyme release is decreased by adding ATP to the specimen in vitro or in hypertonic solution. Imipramine inhibits the capping phenomenon (an aggregation of antigen/antibody complexes of the membrane) of human B lymphocytes labeled with fluorescein-conjugated antihuman immunoglobulins. Serotonin alone has no such effect, but, administered together with imipramine, it potentiates the inhibition of capping by imipramine.
细胞内大分子释放增加导致血浆酶活性高于正常水平，这是杜氏肌营养不良症的一个重要诊断特征。当给大鼠服用丙咪嗪和血清素时，这种疾病的这些以及其他生化和组织学特征会如实地重现。丙咪嗪而非单独的血清素，会导致大鼠膈肌和人类淋巴细胞释放酶，以及在体外导致红细胞释放血红蛋白。哇巴因则不会导致这些情况。在体外或高渗溶液中向标本中添加ATP可减少丙咪嗪诱导的酶释放。丙咪嗪抑制用荧光素标记的抗人免疫球蛋白标记的人B淋巴细胞的帽化现象（膜上抗原/抗体复合物的聚集）。单独的血清素没有这种作用，但与丙咪嗪一起给药时，它会增强丙咪嗪对帽化的抑制作用。
