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首页> 外文期刊>Life sciences >CHOLINERGIC CONTROL OF CEREBRAL BLOOD FLOW IN STROKE, TRAUMA AND AGING
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CHOLINERGIC CONTROL OF CEREBRAL BLOOD FLOW IN STROKE, TRAUMA AND AGING

机译：卒中，创伤和衰老中脑血流的胆碱控制

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Enhancing the availability of endogenous acetylcholine by inhibition of cholinesterase with physostigmine, eptastigmine or soman at sub-toxic doses increases cerebral blood flow (CBF) and the response of this variable to changes in PaCO2. These effects are not correlated with metabolic activation, suggesting that the function of the cholinergic vasodilatation is not merely to supply metabolic substrates. Since choline (Ch) can exchange between blood and the brain extracellular milieu the stage is set for possible feedback interactions between ACh synthesis and CBF. A negative feedback of CBF on ACh synthesis under conditions of a negative arteriovenous (A-V) difference for Ch across cerebral capillaries may contribute to stabilize CBF in ischemia. Eptastigmine and physostigmine significantly improve perfusion in experimental models of focal cerebral ischemia and traumatic brain injury respectively. During the short periods of time in which the A-V difference for Ch across the brain is positive, a positive feedback between cerebral free Ch and CBF may enhance the ability of the brain to recover Ch from the circulation for synthesis of membrane phospholipids. A loss of cholinergic cerebrovascular control may thus impair the survival of all cells within the CNS and contribute to the pathophysiology of dementia. Perhaps the view that the loss of cholinergic cells is the end point of Alzheimer's dementia could be modified to state that a cholinergic deficit may be the starting point of a decline in cerebral phospholipid turnover and cell membrane renewal that could lead to a generalized deterioration of cerebral function. [References: 44]
机译：通过使用毒扁豆碱，依他斯汀明或梭曼抑制亚胆碱剂量的胆碱酯酶来提高内源性乙酰胆碱的利用率可增加脑血流量（CBF），并且该变量对PaCO2变化的反应。这些作用与代谢活化无关，这表明胆碱能血管舒张的功能不仅仅是提供代谢底物。由于胆碱（Ch）可以在血液和大脑细胞外环境之间交换，因此为ACh合成和CBF之间可能的反馈相互作用设定了阶段。在脑毛细血管的Ch负动静脉（A-V）差异的条件下，CBF对ACh合成的负反馈可能有助于稳定缺血中的CBF。依他斯的明和毒扁豆碱分别在局灶性脑缺血和脑外伤实验模型中显着改善灌注。在整个大脑中Ch的A-V差异为正的短时间内，大脑游离Ch和CBF之间的正反馈可能会增强大脑从循环中恢复Ch的能力，以合成膜磷脂。胆碱能脑血管控制的丧失可能因此损害中枢神经系统内所有细胞的存活并有助于痴呆的病理生理学。胆碱能细胞丧失是阿尔茨海默氏痴呆症的终点的观点可能被修改为陈述，胆碱能缺乏可能是脑磷脂更新和细胞膜更新下降的起点，可能导致脑部普遍性退化功能。 [参考：44]

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