Derias N W, Adams C W
J Clin Pathol. 1982 Apr;35(4):407-9. doi: 10.1136/jcp.35.4.407.
The histochemical creatine phosphokinase (CPK) tetrazolium test has been evaluated to detect recent human myocardial infarction in gross slices of the heart at necropsy. The demonstration of the lesion with this method has been assumed to result from local loss of CPK from the damaged myocardium. However, the present study indicates that the mechanism involved depends on localising NADPH tetrazolium reductase and not CPK. Phenazine methosulphate (PMS), when added to the incubating medium as an electron-acceptor to circumvent the tetrazolium-reductase (diaphorase) system, resulted in generalised false staining of the heart slice.
已对尸检时心脏大体切片中用于检测近期人类心肌梗死的组织化学肌酸磷酸激酶（CPK）四氮唑试验进行了评估。用这种方法显示病变被认为是由于受损心肌中CPK局部丧失所致。然而，本研究表明所涉及的机制取决于定位NADPH四氮唑还原酶而非CPK。当作为电子受体加入孵育培养基中以规避四氮唑还原酶（黄递酶）系统时，硫酸吩嗪甲酯（PMS）导致心脏切片出现普遍的假染色。
