Hermansen K, Schmitz O, Arnfred J, Mogensen C E
Diabetes Res. 1986 May;3(4):221-3.
Antihypertensive treatment with furosemide and indapamide may eventually cause impairment of glucose metabolism. To study if this was due to a direct effect on the endocrine pancreas, we examined the effects of furosemide and indapamide on the release of insulin and somatostatin from the isolated perfused pancreas of normal dogs. Furosemide at concentrations ranging between 1-30 micrograms/ml inhibited insulin in a dose-dependent manner (2p less than 0.01) whereas the somatostatin secretion was left unchanged. Also the infusion of indapamide at doses ranging between 0.05-1 micrograms/ml subdued B-cell secretion at the two highest concentrations of 0.5 (by 15 +/- 2%, p less than 0.01) and 1 microgram/ml (by 22 +/- 5%, p less than 0.02) while pancreatic D-cell secretion did not alter. The results suggest, that furosemide and indapamide possess the ability to directly inhibit insulin secretion. Whether this effect is of clinical importance for the diminution in glucose tolerance observed during therapy remains, however, uncertain.
使用呋塞米和吲达帕胺进行抗高血压治疗最终可能会导致葡萄糖代谢受损。为了研究这是否是由于对内分泌胰腺的直接作用，我们检测了呋塞米和吲达帕胺对正常犬离体灌注胰腺释放胰岛素和生长抑素的影响。浓度在1 - 30微克/毫升之间的呋塞米以剂量依赖方式抑制胰岛素（P<0.01），而生长抑素分泌未发生变化。同样，剂量在0.05 - 1微克/毫升之间的吲达帕胺输注在最高的两个浓度0.5微克/毫升（降低15±2%，P<0.01）和1微克/毫升（降低22±5%，P<0.02）时抑制B细胞分泌，而胰腺D细胞分泌未改变。结果表明，呋塞米和吲达帕胺具有直接抑制胰岛素分泌的能力。然而，这种作用对于治疗期间观察到的葡萄糖耐量降低是否具有临床重要性仍不确定。
