Stoner H B, Hunt A
Brain Res. 1976 Aug 13;112(2):337-46. doi: 10.1016/0006-8993(76)90288-2.
Changes in the concentration of the main noradrenaline metabolite in rat brain, 4-hydroxy-3-methoxy-phenylethyleneglycol sulphate (MOPEG-SO4) have been studied during and after injury by limb ischaemia. In the hypothalamus the MOPEG-SO4 concentration rose in about 30 min to a new plateau level which was maintained during a 4 h period of bilateral hind-limb ischaemia and then rose further when the circulation to the limbs was restored. After about 2 h hind-limb ischaemia the concentration in the hind-brain, particularly in the caudal half, rose progressively and this rise continued when the tourniquets were removed after 4 h. Limb ischaemia did not affect the MOPEG-SO4 concentration in the cerebellum but the concentration rose in the cerebrospinal fluid. Attempts to study the production of MOPEG-SO4 in more detail by inhibiting its transport from the brain with probenecid were not helpful and reasons are given for thinking that probenecid is not a useful tool for this type of investigation. The results are considered to provide further evidence that trauma activates ascending and descending pathways which arise from the noradrenergic nerve cells in the hind-brain.
在大鼠肢体缺血损伤期间及损伤后,对大鼠脑内主要去甲肾上腺素代谢产物4-羟基-3-甲氧基苯乙二醇硫酸盐(MOPEG-SO4)的浓度变化进行了研究。在双侧后肢缺血4小时期间,下丘脑的MOPEG-SO4浓度在约30分钟内升至新的稳定水平,并在该期间保持稳定,随后在恢复肢体循环时进一步升高。后肢缺血约2小时后,后脑尤其是后半部的浓度逐渐升高,在4小时后松开止血带时,这种升高仍在继续。肢体缺血未影响小脑的MOPEG-SO4浓度,但脑脊液中的浓度升高。试图通过丙磺舒抑制其从脑内的转运来更详细地研究MOPEG-SO4的产生,但未取得成效,并给出了认为丙磺舒不是此类研究有用工具的原因。这些结果被认为进一步证明了创伤激活了源自后脑去甲肾上腺素能神经细胞的上行和下行通路。