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本实验采用双侧颈总动脉夹闭（ＣＣＡＯ）和大脑中动脉闭塞（ＭＣＡＯ）两种脑缺血动物模型，分别用乙酰胆碱（ＡＣｈ）生物测定法检测皮层ＡＣｈ含量，ＡＣｈ离子选择性微电极（ＡＣｈ－ＩＳＭｓ）检测皮层ＡＣｈ释放量，乙酰胆碱酯酶（ＡＣｈＥ）生化测定法检测皮层ＡＣｈＥ活性，观察脑缺血时皮层ＡＣｈ含量的动态查化。结果发现：脑缺血可诱发皮层ＡＣｈ活度急剧上升，示ＡＣｈ突然大量释放，在ＣＣＡＯ组于缺血１０ｍｉｎ达到高峰（净增１．４４４ｍｍｏｌ／Ｌ），而ＭＣＡＯ组于缺血２ｍｉｎ即达高峰（净增１．５５３ｍｍｏｌ／Ｌ），随着缺血延长，二者均逐渐下降，于缺血３０ｍｉｎ时，虽较峰值要低，但明显高于缺血前水平，此时，ＡＣｈＥ活性巳明显低于缺血前，ＡＣｈ含量在ＣＣＡＯ组下降０．２５６μｇ／ｇ（Ｐ＞０．０５），在ＭＣＡＯ组则显著下降１．０１４μｇ／ｇ（Ｐ＜０．０１）。结果提示：皮层ＡＣｈ含量变化对缺血是敏感的；脑缺血时ＡＣｈ含量下降、释放增加、降解减弱，推测ＡＣｈ可能在缺血性脑损伤中起重要作用。
In this study, two cerebral ischemic models of bilateral common carotid artery occlusion (CCAO) and middle cerebral artery occlusion (MCAO) were established. Acetylcholine (ACh) bioassay was used to detect the cortical ACh content, ACh ion-selective microelectrode ACh-ISMs) were used to detect the ACh release in the cortex. The acetylcholinesterase (AChE) biochemical assay was used to detect the AChE activity in the cortex. The results showed that the activity of ACh in cortex increased sharply after cerebral ischemia, which showed a sudden release of ACh. The peak of ACh peaked at 10 min after ischemia in ischemia-reperfusion group (1.444 mmol / L net increase), while peaked at 2 min in MCAO group (Net increase of 1.553mmol / L). With the prolongation of ischemia, both of them decreased gradually. Although they were lower than the peak at 30min ischemia, they were obviously higher than the pre-ischemic level, and AChE activity was obviously Before ischemia, ACh content decreased by 0.256μg / g in CCAO group and 1.014μg / g in MCAO group (P <0.01). The results suggest that the change of cortical ACh content is sensitive to ischemia; the content of ACh decreases, the release increases, and the degeneration of ACh decreases. It is speculated that ACh may play an important role in ischemic brain injury.