LaManna J C, Cordingley G, Rosenthal M
J Pharmacol Exp Ther. 1977 Mar;200(3):560-9.
Extracellular potassium activity and changes in the reduction levels of intramitochondrial pyridine nucleotide (NAD) and cytochrome-a,a3 were monitored in the cerebral cortex of cats at rest and during electrical stimulation, before and after administration of sodium phenobarbital. Stimulation of the cortical surface evoked a transient increase in the level of oxidized NAD which was proportional in magnitude to the associated transient elevation of extracellular potassium. Phenobarbital (i.v.) produced, within minutes, a persistent shift in NAD to a more reduced level indicative of decreased oxygen consumption. Electrical excitability of the cortex also decreased within minutes, although there was no concomitant change in the resting extracellular potassium activity. Cortical stimulation produced transient elevations of [K+]0 and NADH oxidation and these responses returned to base lines more slowly following the barbiturate administration. However, the proportionality between NADH oxidation and [K+]0 elevation was not altered by phenobarbital. The kinetics of the cytochrome-a, a3 response to cortical stimulation mirrored those of NADH, implying that phenobarbital was not blocking electron transport in the respiratory chain between NADH and cytochrome-a, a3 even at doses where "resting" tissue oxygen consumption was decreased. The prolongation of recovery metabolism following phenobarbital was interpreted as being the result of protracted elevation of extracellular potassium activity. The slow return to "resting" levels of extracellular potassium is probably caused by interference with passive clearance mechanisms.
在静息状态以及电刺激期间，于注射苯巴比妥钠前后，监测猫大脑皮质细胞外钾活性以及线粒体内吡啶核苷酸（NAD）和细胞色素 - a,a3还原水平的变化。刺激皮质表面会引起氧化型NAD水平短暂升高，其幅度与细胞外钾的相关短暂升高成比例。静脉注射苯巴比妥钠在数分钟内会使NAD持续向更还原的水平转变，这表明氧消耗减少。皮质的电兴奋性在数分钟内也会降低，尽管静息细胞外钾活性没有伴随变化。皮质刺激会使[K⁺]₀和NADH氧化短暂升高，在注射巴比妥酸盐后，这些反应恢复到基线的速度更慢。然而，苯巴比妥并未改变NADH氧化与[K⁺]₀升高之间的比例关系。细胞色素 - a,a3对皮质刺激的反应动力学与NADH的反应动力学相似，这意味着即使在“静息”组织氧消耗降低的剂量下，苯巴比妥也不会阻断呼吸链中NADH与细胞色素 - a,a3之间的电子传递。苯巴比妥给药后恢复代谢的延长被解释为细胞外钾活性持续升高的结果。细胞外钾缓慢恢复到“静息”水平可能是由于被动清除机制受到干扰所致。
