Koskinen L D, Sperber G O
Acta Physiol Scand. 1986 Mar;126(3):349-53. doi: 10.1111/j.1748-1716.1986.tb07826.x.
The local cerebral metabolism in urethane anaesthetized control and TRH-treated rabbits was studied with the [14C]2-deoxyglucose method. In the controls, the glucose use was found to be highest in regions known to have a high blood flow and low in regions with low flow. The glucose consumption was, calculated using the constants found by Kennedy et al. in monkeys, 23.5 +/- 6.0 mumol 100 g-1 min-1 in parietal cortex. The TRH was infused at a dose of 0.06 mg kg-1 min-1 which is known to cause vasodilation in the brain. No marked influence of the peptide on the glucose use was detected. It was concluded that the previously reported cerebral vasodilation caused by TRH is not due to an increase in cerebral metabolism.
采用[14C]2-脱氧葡萄糖法研究了氨基甲酸乙酯麻醉的对照兔和TRH处理兔的局部脑代谢。在对照兔中,发现葡萄糖利用在已知血流高的区域最高,在血流低的区域最低。根据肯尼迪等人在猴子身上发现的常数计算,顶叶皮质的葡萄糖消耗量为23.5±6.0 μmol 100 g-1 min-1。以0.06 mg kg-1 min-1的剂量输注TRH,已知该剂量会引起脑血管舒张。未检测到该肽对葡萄糖利用有明显影响。得出的结论是,先前报道的由TRH引起的脑血管舒张并非由于脑代谢增加所致。