Saccà L, Perez G
Metabolism. 1976 Feb;25(2):127-30. doi: 10.1016/0026-0495(76)90041-x.
The effect of PGE1and PGA1 intravenous infusion (2/mug/min) on plasma glucose and glucagon levels was investigated in normal, sympathectomized and propranolol-treated rats. PGE1 infusion significantly increased glucose and glucagon levels, while PGA1 had no effect. Since the dose of PGE1 used in this study was able to reduce the arterial blood pressure by about 20%, the possibility that PGE1 acted indirectly through a reflex sympathetic overactivity was tested. The increases in plasma glucagon induced by PGE1 occurred also in sympathectomized or in beta-blocked animals. Thus, it was possible to exclude a sympathetic mediation or a direct stimulation of pancreatic beta-receptors as a likely mechanism of PGE1 action.
在正常、去交感神经和普萘洛尔处理的大鼠中，研究了静脉输注前列腺素E1（PGE1）和前列腺素A1（PGA1）（2微克/分钟）对血糖和胰高血糖素水平的影响。输注PGE1可显著提高血糖和胰高血糖素水平，而PGA1则无此作用。由于本研究中使用的PGE1剂量能够使动脉血压降低约20%，因此对PGE1是否通过反射性交感神经过度活动间接起作用进行了测试。PGE1诱导的血浆胰高血糖素升高在去交感神经或β受体阻断的动物中也会出现。因此，可以排除交感神经介导或直接刺激胰腺β受体作为PGE1作用的可能机制。
