去甲肾上腺素耗竭会改变“活跃”状态下的脑氧化代谢。

Norepinephrine depletion alters cerebral oxidative metabolism in the "active" state.

作者信息

LaManna J C, Harik S I, Light A I, Rosenthal M

出版信息

Brain Res. 1981 Jan 5;204(1):87-101. doi: 10.1016/0006-8993(81)90654-5.

Abstract

Unilateral chemical lesion of the nucleus locus coeruleus in rats produced unilateral depletion of ipsilateral cortical norepinephrine. Norepinephrine depletion was not associated with changes in "resting" metabolic balance of the cerebral cortex, as determined by in situ reflection spectrophotometry of the redox state of cytochrome oxidase. Norepinephrine depletion, however, caused slowing of the transient metabolic response to sudden increases in energy demand produced by direct cortical electrical stimulation. The effect was apparent in the redox state of both cytochrome oxidase and NAD, the latter being measured, also in situ, by reflection microfluorometry. These results demonstrate that norepinephrine has a role in modulating the response to increased metabolic demand in the cerebral cortex. Norepinephrine may mediate its effect by potentiating Na+, K+-ATPase or through its effects on vascular reactivity, or both.

摘要

大鼠蓝斑核的单侧化学损伤导致同侧皮质去甲肾上腺素的单侧耗竭。通过对细胞色素氧化酶氧化还原状态的原位反射分光光度法测定，去甲肾上腺素耗竭与大脑皮质“静息”代谢平衡的变化无关。然而，去甲肾上腺素耗竭导致对直接皮质电刺激产生的能量需求突然增加的瞬时代谢反应减慢。这种效应在细胞色素氧化酶和NAD的氧化还原状态中都很明显，后者也是通过反射显微荧光测定法原位测量的。这些结果表明，去甲肾上腺素在调节大脑皮质对增加的代谢需求的反应中起作用。去甲肾上腺素可能通过增强Na +、K + -ATP酶或通过其对血管反应性的影响，或两者兼而有之来介导其作用。