OXYGEN AND GLUCOSE CONSUMPTION RELATED TO NA+-K+ TRANSPORT IN CANINE BRAIN
OXYGEN AND GLUCOSE CONSUMPTION RELATED TO NA+-K+ TRANSPORT IN CANINE BRAIN
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DOI：
10.1161/01.str.12.6.726
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发表时间：
1981-01-01
期刊：
影响因子：
8.3
通讯作者：
SORENSEN, HR
中科院分区：
文献类型：
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作者：
ASTRUP, J;SORENSEN, PM;SORENSEN, HR
研究了Na+-K+转运与犬脑代谢的关系。采用矢状窦流出技术测定脑氧和葡萄糖消耗。戊巴比妥40 mg/kg （EEG平）阻断突触传递及相关代谢。利多卡因阻断了另外15-20%，可能是通过限制Na+-K+泄漏通量和减少Na+-K+运输的需求。瓦巴因又阻断了20-25%的新陈代谢。瓦巴因抑制了Na+-K+敏感的atp酶相关的转运，并导致K+从细胞室净流出，这可以从皮层细胞外K+浓度的增加中得到证明。巴比妥酸盐抑制脑电图的大脑中有40%的代谢可能与Na+-K+泄漏通量和相关运输有关。其余60%与本研究未确定的过程有关。脑代谢可能降低到巴比妥最低限度以下。
The relation between Na+-K+ transport and metabolism in the canine brain was studied. Cerebral O2 and glucose consumption was measured by the sagittal sinus outflow technique. Synaptic transmission and related metabolism was blocked by pentobarbital 40 mg/kg (EEG flat). Lidocaine blocked an additional 15-20%, presumably by restricting Na+-K+ leak fluxes and reducing the demand for Na+-K+ transport. Ouabain blocked an additional 20-25% of metabolism. Ouabain inhibited the Na+-K+ sensitive ATPase associated transport and caused a net efflux of K+ from the cellular compartment as evidenced by an increasing extracellular K+ concentration in the cortex. A total of 40% of metabolism in the EEG-arrested barbiturate inhibited brain could be related to Na+-K+ leak fluxes and associated transport. The remaining 60% are related to processes unidentified by this study. Cerebral metabolism may be reduced below the hitherto described barbiturate minimum.