Andersson M, Hanson A, Englund G, Dahlbäck B
Department of Clinical Chemistry, University of Lund, Malmö General Hospital, Sweden.
Eur J Clin Pharmacol. 1991;40(3):261-5. doi: 10.1007/BF00315206.
The effect of cadralazine and its active metabolite CGP 22639 on the covalent binding reaction of C4 and C3 has been studied. Trypsin-Sepharose was used to activate radio-labelled C3 and C4 and binding of the radio-labelled protein to the trypsin-Sepharose was measured. Cadralazine inhibited 50% of the binding of C3 and C4 at concentrations of 19 mmol/l and 15 mmol/l, respectively. Its active metabolite was more potent and inhibited 50% of the C3 and C4 binding at concentrations of 8 and 3.5 mmol/l, respectively. These concentrations are much higher than those found in plasma during therapy. This is consistent with the clinical observation that in patients with normal kidney function cadralazine is not an inducer of SLE.
已研究了卡屈嗪及其活性代谢物CGP 22639对C4和C3共价结合反应的影响。使用胰蛋白酶-琼脂糖凝胶来激活放射性标记的C3和C4，并测定放射性标记蛋白与胰蛋白酶-琼脂糖凝胶的结合。卡屈嗪分别在19 mmol/l和15 mmol/l的浓度下抑制了50%的C3和C4结合。其活性代谢物效力更强，分别在8 mmol/l和3.5 mmol/l的浓度下抑制了50%的C3和C4结合。这些浓度远高于治疗期间血浆中的浓度。这与临床观察结果一致，即在肾功能正常的患者中，卡屈嗪不是系统性红斑狼疮的诱导剂。
