Dóra E, Gyulai L, Kovách A G
Brain Res. 1984 May 7;299(1):61-72. doi: 10.1016/0006-8993(84)90788-1.
In order to elucidate that which are the factors that may influence the direction of brain activation-induced changes in the redox state of oxidized/reduced nicotinamide adenine dinucleotide (NAD/NADH), the brain cortex was electrically stimulated during arterial hypotension and following reinfusion of the shed blood, during arterial hyper- and hypoxia, and during the second phase of spreading cortical depression (SD). Cerebrocortical NADH fluorescence and vascular volume ( CVV ) of cats, anaesthetized by chloralose, were measured with a microscope fluororeflectometer . Under physiologically normal conditions electrical stimulation resulted in pronounced cortical NAD reduction and increase in CVV . These reactions were not altered by arterial hyperoxia and continuous superfusion of the brain cortex with oxygenated artificial cerebrospinal fluid (mock CSF). Arterial hypotension and SD (in phase II) increased NAD reduction and CVV markedly, and the superimposed electrical stimulation brought about NADH oxidation and greatly depressed CVV responses. Reinfusion of the shed blood did not restore NAD/NADH redox state and CVV to their reference levels, and electrical stimulation under this condition led to NADH oxidation and negligible vascular reactions. Since under physiologically normal conditions electrical activation of the brain cortex resulted in NAD reduction and marked increase in CVV and the magnitude of these reactions were not altered by arterial hyperoxia or by superfusion of the brain cortex with oxygenated CSF, it is very unlikely that the brain cortex became hypoxic during stimulation. Because when the steady NAD/NADH redox state of the brain cortex was shifted toward reduction by arterial hypotension and reinfusion and SD, electrical stimulation led to NADH oxidation, it is suggested that the prestimulatory steady redox state has great importance in determining the direction of NAD/NADH redox reactions evoked by activation of the brain cortex.
为了阐明哪些因素可能影响脑激活诱导的氧化型/还原型烟酰胺腺嘌呤二核苷酸（NAD/NADH）氧化还原状态变化的方向，在动脉低血压期间、回输失血后、动脉高氧和缺氧期间以及皮层扩展性抑制（SD）的第二阶段，对大脑皮层进行电刺激。用显微镜荧光反射仪测量用氯醛糖麻醉的猫的大脑皮层NADH荧光和血管容积（CVV）。在生理正常条件下，电刺激导致皮层NAD明显减少，CVV增加。这些反应不受动脉高氧和用含氧人工脑脊液（模拟脑脊液）持续灌注大脑皮层的影响。动脉低血压和SD（第二阶段）显著增加NAD减少和CVV，叠加的电刺激导致NADH氧化并极大地抑制CVV反应。回输失血并未使NAD/NADH氧化还原状态和CVV恢复到参考水平，在此条件下的电刺激导致NADH氧化和可忽略不计的血管反应。由于在生理正常条件下大脑皮层的电激活导致NAD减少和CVV显著增加，且这些反应的幅度不受动脉高氧或用含氧脑脊液灌注大脑皮层的影响，因此在刺激期间大脑皮层变得缺氧的可能性非常小。因为当大脑皮层稳定的NAD/NADH氧化还原状态因动脉低血压、回输和SD而向还原方向转变时，电刺激导致NADH氧化，所以提示刺激前的稳定氧化还原状态在确定大脑皮层激活诱发的NAD/NADH氧化还原反应方向方面具有重要意义。
