Matsui Y, Ishibashi H, Kimura K, Shiota M, Ohta M, Sugano T
Laboratory of Veterinary Physiology, University of Osaka Prefecture, Japan.
Am J Physiol. 1993 Jul;265(1 Pt 2):R117-23. doi: 10.1152/ajpregu.1993.265.1.R117.
The responses of hepatic glycogenolysis to catecholamines in ventromedial hypothalamus (VMH)-lesioned male rats were examined in perfused livers. Seven days after bilateral electrical lesioning of the VMH, the livers were perfused. Isoproterenol, a beta-agonist, stimulated greater glucose production in VMH-lesioned rats than in controls (32.8 vs. 5.6 mumol glucose.h-1.g liver-1), while responses to phenylephrine, an alpha-agonist, decreased significantly compared with controls (44.4 vs. 69.8 mumol glucose.h-1.g liver-1). There were no significant differences in responses of livers to glucagon and vasopressin between control and VMH-lesioned rats. Adrenodemedullation showed the same effect on beta-responses as lesions in the VMH, but no effect on alpha-responses. Plasma epinephrine levels were not detectable with the high-performance liquid chromatography analysis in VMH-lesioned rats. The periodicity of plasma corticosterone levels was observed in both VMH-lesioned and control rats, although daytime increases in plasma corticosterone were blocked by VMH lesions. These results suggest that the lesions in the VMH cause changes in the levels of adrenergic receptor and that the increase in beta-responses is caused mostly by the reduction of plasma epinephrine.
在灌注肝脏中研究了腹内侧下丘脑（VMH）损伤的雄性大鼠肝脏糖原分解对儿茶酚胺的反应。VMH双侧电损伤7天后，对肝脏进行灌注。β-激动剂异丙肾上腺素刺激VMH损伤大鼠产生的葡萄糖比对照组更多（分别为32.8与5.6 μmol葡萄糖·h⁻¹·g肝脏⁻¹），而与对照组相比，α-激动剂去氧肾上腺素的反应显著降低（分别为44.4与69.8 μmol葡萄糖·h⁻¹·g肝脏⁻¹）。对照组和VMH损伤大鼠肝脏对胰高血糖素和血管加压素的反应没有显著差异。肾上腺髓质切除对β反应的影响与VMH损伤相同，但对α反应没有影响。通过高效液相色谱分析在VMH损伤大鼠中未检测到血浆肾上腺素水平。在VMH损伤大鼠和对照大鼠中均观察到血浆皮质酮水平的周期性，尽管VMH损伤阻断了白天血浆皮质酮的升高。这些结果表明，VMH损伤导致肾上腺素能受体水平发生变化，并且β反应的增加主要是由血浆肾上腺素的减少引起的。
