Savaki H E, McCulloch J, Kadkaro M, Sokoloff L
Brain Res. 1982 Feb 11;233(2):347-58. doi: 10.1016/0006-8993(82)91207-0.
The energy metabolism of the central nervous structures involved in the regulation of blood pressure was examined by means of the autoradiographic 2-deoxy-D-[14C]glucose method in normal, awake rats during hypotension induced by the alpha-adrenergic blockers, phentolamine, phenoxybenzamine, and yohimbine. Administration of these alpha-blockers produced a dose-dependent increase of glucose consumption in the medial nucleus of the solitary tract (NTSm), the dorsal motor nucleus of the vagus (DMX), the nucleus ambiguus (NA), and the paraventricular (PAVH) and supraoptic (SO) hypothalamic nuclei. However, in the external cuneate nucleus and in the paramedian reticular nucleus there was a decrease in glucose utilization. These changes appear to be at least partly due to the hypotension produced by the drugs in addition to their central effects; when the hypotension was prevented by administration of the plasma expander, dextran, in phenoxybenzamine-treated rats, the effects were less than those observed in animals with hypotension not limited by dextran infusion.
在正常清醒大鼠中,通过放射自显影2-脱氧-D-[14C]葡萄糖法,研究了在α-肾上腺素能阻滞剂酚妥拉明、酚苄明和育亨宾诱导低血压期间,参与血压调节的中枢神经结构的能量代谢。给予这些α-阻滞剂后,孤束核内侧核(NTSm)、迷走神经背运动核(DMX)、疑核(NA)以及下丘脑室旁核(PAVH)和视上核(SO)的葡萄糖消耗量呈剂量依赖性增加。然而,楔外核和旁正中网状核的葡萄糖利用率降低。这些变化似乎至少部分是由于药物除了其中心作用外还产生了低血压;当在酚苄明处理的大鼠中通过给予血浆扩容剂右旋糖酐来预防低血压时,其作用小于在未受右旋糖酐输注限制的低血压动物中观察到的作用。