Roald O K, Steen P A, Milde J H, Michenfelder J D
Acta Anaesthesiol Scand. 1986 May;30(4):341-5. doi: 10.1111/j.1399-6576.1986.tb02427.x.
In six dogs initially anesthetized with halothane-N2O-O2 for surgery and maintained during the experiment with high spinal anesthesia and local infiltration, diazepam 3.0 mg X kg-1 converted the EEG from an awake to a sleep pattern. This was accompanied by a significant 21% reduction in cerebral metabolic rate for oxygen (CMRO2) and a 15% reduction in cerebral blood flow (CBF). Substituting nitrous oxide 70% for nitrogen had no additional cerebral effects. The benzodiazepine antagonist Ro15-1788, 2 mg, completely reversed the effects of diazepam on the EEG, CMRO2 and CBF. Cerebral biopsies taken at the end of the study revealed modest but significant decreases in ATP and the energy charge along with increases in AMP, lactate and lactate/pyruvate (L/P) ratio. These changes are unexplained and suggest a possible disturbance in oxidative phosphorylation produced by Ro15-1788 preceded by diazepam.
在六只最初用氟烷 - N₂O - O₂麻醉以进行手术并在实验期间用高位脊髓麻醉和局部浸润维持麻醉的狗中，3.0毫克/千克的地西泮使脑电图从清醒模式转变为睡眠模式。这伴随着脑氧代谢率（CMRO₂）显著降低21%以及脑血流量（CBF）降低15%。用70%的氧化亚氮替代氮气没有额外的脑效应。2毫克苯二氮䓬拮抗剂Ro15 - 1788完全逆转了地西泮对脑电图、CMRO₂和CBF的作用。研究结束时进行的脑活检显示，ATP和能量电荷适度但显著降低，同时AMP、乳酸和乳酸/丙酮酸（L/P）比值增加。这些变化无法解释，提示在Ro15 - 1788之前地西泮可能导致了氧化磷酸化的干扰。
