Levin B E, Sullivan A C
Neurology Service, Veterans Administration, E. Orange, NJ 07019.
J Auton Nerv Syst. 1987 Oct;20(3):233-42. doi: 10.1016/0165-1838(87)90152-4.
Selective activation of the two components of the sympatho-adrenal system (SAS) was produced by infusing male Sprague-Dawley rats with glucose or insulin. Intravenous glucose (0.5, 1 or 2 g/kg) raised plasma levels of glucose and insulin associated with a predominant activation of the sympathetic nervous system (SNS) as indicated by increased plasma norepinephrine (NE) levels. Glucose-induced release of NE was still seen in hypoinsulinemic, streptozotocin-treated rats but was absent after ganglionic blockade with chlorisondamine or following mannitol or saline infusions which failed to alter glucose or insulin levels. Insulin-induced (10 or 20 U/kg) hyperinsulinemia with its associated hypoglycemia produced predominant activation of the adrenal medulla producing increased plasma epinephrine (E) levels. But significant SNS activation also occurred with a concomitant increase in NE levels (14-22% of E) which appeared to be primarily from sympathetic nerves since increases still occurred following adrenal demedullectomy. Therefore, changes in plasma glucose levels alone and possibly altered intracellular concentrations or rates of glucose utilization can act as an important determinant of the pattern SAS activation although this may require pathological changes in plasma glucose levels to occur.
通过给雄性斯普拉格-道利大鼠输注葡萄糖或胰岛素,实现了对交感-肾上腺系统(SAS)两个组成部分的选择性激活。静脉注射葡萄糖(0.5、1或2 g/kg)可提高血浆葡萄糖和胰岛素水平,同时交感神经系统(SNS)被显著激活,表现为血浆去甲肾上腺素(NE)水平升高。在低胰岛素血症的链脲佐菌素处理大鼠中仍可见葡萄糖诱导的NE释放,但在用氯异吲哚铵进行神经节阻断后,或在输注甘露醇或生理盐水未能改变葡萄糖或胰岛素水平后,NE释放消失。胰岛素诱导(10或20 U/kg)的高胰岛素血症及其相关的低血糖主要激活肾上腺髓质,导致血浆肾上腺素(E)水平升高。但同时也发生了显著的SNS激活,NE水平随之增加(占E的14 - 22%),这似乎主要来自交感神经,因为在肾上腺髓质切除术后NE水平仍会升高。因此,仅血浆葡萄糖水平的变化以及可能改变的细胞内葡萄糖浓度或利用率,都可作为SAS激活模式的重要决定因素,尽管这可能需要血浆葡萄糖水平发生病理变化。