Padhani A, Turaihi K, Junglee D, Menon R K, Dandona P
Department of Chemical Pathology and Human Metabolism, Royal Free Hospital and School of Medicine, London, U.K.
Agents Actions. 1987 Oct;22(1-2):131-3. doi: 10.1007/BF01968828.
To elucidate whether indomethacin-induced hyperkalaemia is due to an inhibition of Na-K ATPase in the membranes, indomethacin (25 mg t.d.s.) was administered to 7 normal subjects for 7 days. This resulted in an increase in plasma potassium concentrations in all 7 subjects: median (range) for the entire group increased from 4.19 (3.98-4.79) mmol/l to 4.29 (4.13-4.87) mmol/l. Leucocytes prepared from these subjects prior to and after indomethacin were tested for 86Rb influx and [3H]-ouabain binding (an index of Na-K ATPase sites). Neither 86Rb influx (total, ouabain sensitive and ouabain insensitive) nor [3H]-ouabain binding changed significantly following indomethacin. We conclude that (a) indomethacin-induced hyperkalaemia is not due to alterations in potassium influx into cells and (b) the modulation of Na-K ATPase sites/activity is in leucocytes not dependent upon prostaglandins.
为阐明消炎痛诱导的高钾血症是否是由于细胞膜中钠钾ATP酶受到抑制，对7名正常受试者给予消炎痛（每日3次，每次25毫克），持续7天。这使得所有7名受试者的血浆钾浓度均升高：整个组的中位数（范围）从4.19（3.98 - 4.79）毫摩尔/升增至4.29（4.13 - 4.87）毫摩尔/升。对这些受试者在服用消炎痛前后制备的白细胞进行了⁸⁶Rb内流和[³H] - 哇巴因结合（钠钾ATP酶位点的一个指标）测试。服用消炎痛后，⁸⁶Rb内流（总量、哇巴因敏感和哇巴因不敏感）以及[³H] - 哇巴因结合均未发生显著变化。我们得出结论：（a）消炎痛诱导的高钾血症并非由于钾流入细胞的改变所致；（b）白细胞中钠钾ATP酶位点/活性的调节不依赖于前列腺素。
