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严重胰岛素诱导低血糖期间猫的脑氧化还原状态

The cerebral redox state in cats during severe insulin induced hypoglycemia.

作者信息

Bryan R M, Jobsis F F

出版信息

Brain Res. 1983 Nov 21;279(1-2):266-70. doi: 10.1016/0006-8993(83)90190-7.

Abstract

The cerebral metabolic state was studied in cats during insulin-induced hypoglycemia and the recovery after glucose infusion. Changes in the redox state of nicotinamide adenine dinucleotide (NAD) were monitored from the surface of the exposed cerebral cortex using microfluorometry. After insulin injection blood glucose fell from 6.85 mumol/ml to 0.45 mumol/ml at EEG isoelectricity and was accompanied by an oxidation of NADH+. Upon intravenous glucose infusion EEG activity rapidly returned and NAD became more reduced. The oxidation of NADH+ during severe hypoglycemia demonstrated that the in vivo redox state of mitochondria behave in a similar manner as isolated mitochondria when reducing equivalents become limiting to the respiratory chain.

摘要

在胰岛素诱导的低血糖症及葡萄糖输注后的恢复过程中,对猫的脑代谢状态进行了研究。使用显微荧光测定法从暴露的大脑皮层表面监测烟酰胺腺嘌呤二核苷酸(NAD)氧化还原状态的变化。注射胰岛素后,血糖从6.85 μmol/ml降至脑电图等电位时的0.45 μmol/ml,并伴有NADH⁺的氧化。静脉输注葡萄糖后,脑电图活动迅速恢复,NAD的还原程度增加。严重低血糖期间NADH⁺的氧化表明,当还原当量对呼吸链产生限制时,线粒体在体内的氧化还原状态与分离的线粒体表现相似。

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