Sundt T M, Anderson R E
Stroke. 1975 May-Jun;6(3):279-83. doi: 10.1161/01.str.6.3.279.
The fluorescence of reduced nicotinamide adenine dinucleotide (NADH) from cerebral cortex was measured before, during, and after middle cerebral artery (MCA) occlusion and then at death of the animal. In normal cortex, NADH remained constant throughout a wide range of variations in blood pressure and Paco2. In ischemic cortex, NADH levels were higher in hypovolemic hypotensive animals than in normotensive normovolemic animals. Neither hypercapnia nor hypocapnia was effective in decreasing NADH in regions of ischemia, but the latter was associated with a degree of hypotension that interfered with interpretation of data. NADH returned to normal with restoration of flow, supporting the reversibility of this degree of ischemia. The high levels of NADH at death, compared to those during ischemia, are consistent with incomplete ischemia in this model of cerebral infarction.
在大脑中动脉(MCA)闭塞前、闭塞期间、闭塞后以及动物死亡时,测量大脑皮质中还原型烟酰胺腺嘌呤二核苷酸(NADH)的荧光。在正常皮质中,在血压和动脉血二氧化碳分压(Paco2)的广泛变化范围内,NADH保持恒定。在缺血性皮质中,低血容量性低血压动物的NADH水平高于正常血压、正常血容量动物。高碳酸血症和低碳酸血症均不能有效降低缺血区域的NADH,但后者伴有一定程度的低血压,这干扰了数据的解释。随着血流恢复,NADH恢复正常,支持了这种程度缺血的可逆性。与缺血期间相比,死亡时NADH的高水平与该脑梗死模型中的不完全缺血一致。