Abnormalities of cerebral oxidative metabolism with aging and their relation to the central noradrenergic system.
Abnormalities of cerebral oxidative metabolism with aging and their relation to the central noradrenergic system.
复制标题
衰老引起的脑氧化代谢异常及其与中枢去甲肾上腺素能系统的关系。
DOI：
10.1159/000213124
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发表时间：
1983
期刊：
影响因子：
3.5
通讯作者：
Rosenthal,M
中科院分区：
文献类型：
--
作者：
Sylvia,AL;Harik,SI;LaManna,JC;Wilkerson,T;Rosenthal,M
脑氧化代谢进行了研究，在体内监测细胞色素c氧化酶的氧化还原位移响应于直接电刺激的大脑皮层在Fischer-344大鼠在3个月和28个月的年龄。这种激活导致与局部脑血容量短暂增加相关的细胞色素氧化酶的短暂氧化。在老年大鼠中，与年轻大鼠相比，细胞色素氧化酶的瞬时氧化还原反应（即初始氧化，然后再还原）的速率减慢约50%。两个年龄组的皮质去甲肾上腺素相似。然而，虽然皮质去甲肾上腺素的耗竭导致年轻大鼠的再还原速率减慢约50%，但这种耗竭对老年大鼠氧化还原转变的动力学已经很慢没有影响。血管对代谢需求增加的反应性（由血容量增加与细胞色素氧化的振幅比定义）随年龄增加而增加，但在两个年龄组中因去甲肾上腺素耗竭而减弱。这些结果表明：（1）Fischer-344大鼠大脑皮质的去甲肾上腺素水平不随年龄而下降;（2）大脑氧化代谢对代谢需求增加的条件作出反应的能力出现与年龄有关的损害;（3）这种损害不因大脑去甲肾上腺素的消耗而恶化;（4）对衰老中增加的代谢需求的过度血管反应性表明氧和代谢底物的供应减少，和（5）这种血管反应性由中枢去甲肾上腺素能机制介导。
Cerebral oxidative metabolism was studied in vivo by monitoring redox shifts of cytochrome c oxidase in response to direct electrical stimulation of the cerebral cortex in Fischer-344 rats at 3 and 28 months of age. Such activation results in a transient oxidation of cytochrome oxidase associated with brief increase in local cerebral blood volume. In aged rats, the rates of the transient redox responses of cytochrome oxidase (i.e. initial oxidation followed by re-reduction) are slowed by about 50% in comparison to young rats. Cortical norepinephrine was similar in both age-groups. However, while depletion of cortical norepinephrine causes slowing of the rate of re-reduction in young rats by about 50%, such depletion had no effect on the already slow kinetics of the redox shifts of aged rats. Vascular reactivity to increased metabolic demands, defined by the amplitude ratio of the blood volume increase to the cytochrome oxidation, is increased with age but attenuated by norepinephrine depletion in both age-groups. These results suggest that: (1) cerebral cortical levels of norepinephrine do not decline with age in the Fischer-344 rat; (2) development of an age-related impairment in the capability of cerebral oxidative metabolism to respond to conditions of heightened metabolic demands; (3) such impairment is not worsened by depletion of cerebral norepinephrine; (4) exaggerated vascular reactivity to increased metabolic requirement in aging indicates decreased provision of oxygen and metabolic substrates, and (5) this vascular reactivity is mediated by central noradrenergic mechanisms.