Meilin S, Sonn J, Zarchin N, Rogatsky G, Guggenheimer-Furman E, Mayevsky A
Department of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.
Brain Res. 1998 Jan 12;780(2):323-8. doi: 10.1016/s0006-8993(97)01138-4.
Until recently carbon monoxide (CO) was known only for its noxious effects. Exposure to CO results in an autoregulatory increase in cerebral blood flow (CBF). Little information is available on brain energy metabolism under low CO concentrations and on the effect of CO on the stimulated brain. In this study cortical spreading depression (SD) was induced in order to cause transient brain depolarization and increased energy demand. The multisite assembly (MSA), which contains four bundles of optical fibers for monitoring the intramitochondrial NADH redox state and tissue reflectance as well as four DC electrodes enabling measurement from four consecutive points on the cerebral cortex, was used to measure energy metabolism and the propagation of SD waves during exposure to CO. CBF in the contralateral hemisphere was measured using the laser Doppler technique. Three experimental groups of animals were examined: SD was induced during exposure to 1000 ppm CO, immediately after exposure to CO and 90 min after cessation of exposure to CO. Three control groups were also examined, in which the animals underwent the same procedures but were not exposed to CO. In all animals exposure to CO was followed by a significant increase in CBF. The greatest effect was found when SD was induced immediately after cessation of exposure to CO. SD wave frequency decreased when induced immediately after exposure to CO, whereas it increased when SD was induced 90 min after exposure. The amplitude of the NADH oxidation waves and their integral were smaller during SD induced immediately after exposure to CO. The DC potential did not change, suggesting that CO did not affect the SD initiation mechanism but rather resulted in energy depletion during recovery from SD. This study demonstrates that even at a concentration of 1000 ppm CO interferes with the metabolic activity of the brain during repolarization of the SD-induced negativity.
直到最近，一氧化碳（CO）还仅因其有害影响为人所知。接触CO会导致脑血流量（CBF）自动调节性增加。关于低浓度CO下的脑能量代谢以及CO对受刺激大脑的影响，目前所知甚少。在本研究中，诱导皮层扩散性抑制（SD）以引起短暂的脑去极化并增加能量需求。多部位组件（MSA）包含四束用于监测线粒体内NADH氧化还原状态和组织反射率的光纤以及四个能够从大脑皮层上四个连续点进行测量的直流电极，用于测量暴露于CO期间的能量代谢和SD波的传播。使用激光多普勒技术测量对侧半球的CBF。对三组实验动物进行了检查：在暴露于1000 ppm CO期间、暴露于CO后立即以及停止暴露于CO 90分钟后诱导SD。还检查了三个对照组，其中动物接受相同的程序但未暴露于CO。在所有动物中，接触CO后CBF均显著增加。在停止暴露于CO后立即诱导SD时发现效果最为显著。在暴露于CO后立即诱导SD时，SD波频率降低，而在暴露于CO 90分钟后诱导SD时，SD波频率增加。在暴露于CO后立即诱导SD期间，NADH氧化波的幅度及其积分较小。直流电位没有变化，这表明CO不影响SD起始机制，而是在从SD恢复过程中导致能量消耗。这项研究表明，即使在1000 ppm的浓度下，CO在SD诱导的负电位复极化期间也会干扰大脑的代谢活动。
