Hempel F G, Kariman K, Saltzman H A
Am J Physiol. 1980 Feb;238(2):H249-56. doi: 10.1152/ajpheart.1980.238.2.H249.
Fluorometry and dual-wave-length spectrophotometry were used to detect transitory shifts in the redox state of mitochondrial NADH and cytochrome aa3 in the exposed cerebral cortex of anesthetized paralyzed cats as seizures were induced with pentylenetetrazol. In normotensive animals, NADH and cytochrome aa3 oxidation accompany the seizures, but when the mean arterial pressure (MAP) is reduced to 40.2 +/- 1.1% of the base line by hemorrhaging, the NADH fluorescence response converts to a biphasic oxidation-reduction sequence. In extreme hypotension (MAP lowered to an average of 28%), only NAD reduction transients are observed with seizures, and cytochrome aa3 is oxidized irrespective of the low MAP. Our data show that a reversible perfusion impairment, perhaps inhomogeneous in its distribution, appears in the cortex at the 40% MAP level and modifies electron flux in the respiratory chain between NADH and cytochrome aa3, and uniform oxygen insufficiency is an unlikely cause for the reversal of NADH oxidation toward reduction during seizures under hypovolemic conditions.
在麻醉的瘫痪猫的暴露大脑皮层中，当用戊四氮诱导癫痫发作时，采用荧光测定法和双波长分光光度法检测线粒体NADH和细胞色素aa3氧化还原状态的瞬时变化。在血压正常的动物中，癫痫发作时NADH和细胞色素aa3会发生氧化，但当通过出血使平均动脉压（MAP）降至基线的40.2±1.1%时，NADH荧光反应转变为双相氧化还原序列。在极度低血压（MAP降至平均28%）时，癫痫发作时仅观察到NAD还原瞬变，且无论MAP多低，细胞色素aa3都会被氧化。我们的数据表明，在MAP为40%水平时，皮层中会出现可逆的灌注损伤，其分布可能不均匀，并改变了NADH和细胞色素aa3之间呼吸链中的电子通量，而且在低血容量状态下癫痫发作期间NADH氧化向还原逆转，均匀性氧不足不太可能是其原因。
