Lawrence A M, Ajlouni K, Hagen T C
J Clin Endocrinol Metab. 1984 Oct;59(4):622-4. doi: 10.1210/jcem-59-4-622.
Failure of a plasma glucagon rise in response to insulin-induced hypoglycemia was demonstrated in normal subjects taking therapeutic doses of the nonselective beta-adrenergic blocker, propranolol, for 7 days before testing. This is the first study to examine glucose homeostasis in normal subjects exposed to chronic propranolol therapy and helps to explain the development of spontaneous hypoglycemia in patients, either diabetic or nondiabetic, during beta-adrenergic receptor blockade. Previous studies of the acute parenteral effects of propranolol administration failed to show any significant effect on glucagon secretory dynamics in response to insulin-induced hypoglycemia. In the present study, however, chronic oral administration of propranolol resulted in severe impairment of the expected glucagon rise in response to hypoglycemia and was associated with severe hypoglycemia in one normal subject.
在测试前连续7天服用治疗剂量的非选择性β-肾上腺素能阻滞剂普萘洛尔的正常受试者中,已证实其血浆胰高血糖素对胰岛素诱导的低血糖反应未升高。这是第一项研究慢性普萘洛尔治疗的正常受试者的葡萄糖稳态的研究,有助于解释糖尿病或非糖尿病患者在β-肾上腺素能受体阻断期间自发性低血糖的发生。先前关于普萘洛尔静脉注射急性作用的研究未能显示其对胰岛素诱导的低血糖反应中胰高血糖素分泌动力学有任何显著影响。然而,在本研究中,慢性口服普萘洛尔导致对低血糖反应时预期的胰高血糖素升高严重受损,并且在一名正常受试者中出现了严重低血糖。