全麻药不同程度干扰脑血管功能，或增加脑血氧产生脑保护作用，或致脑组织过度灌注，机制未明。翼腭神经节（PPG）是支配脑血管的副交感神经节；刺激PPG可增加脑血流量。我们发现：全麻药异氟烷可直接激活PPG。已知PPG高表达nAchR胆碱能受体，而异氟烷可结合nAchR跨膜位点。此外，研究表明异氟烷的扩血管效应为一氧化氮（NO）依赖，而PPG中含有大量NO合成酶。据此推测：异氟烷可通过激活PPG的nAchR，释放扩血管物质NO。异氟烷的扩血管效应在糖尿病患者中报道不一。进一步预实验提示：NO合成酶在早、中、晚期糖尿病小鼠的PPG中表达不一致；推测其为异氟烷扩血管效应不一的主因。本课题将结合神经生物学与基因工程学方法，阐述异氟烷通过nAchR释放NO的副交感神经通路特点；剖析糖尿病小鼠PPG的细胞膜受体及神经递质变化对异氟烷扩血管效应的影响；为调控异氟烷的扩血管效应、优化糖尿病患者的麻醉提供依据。

General anesthetics interfere with cerebrovascular function to different degrees. It can increase cerebral blood oxygen to produce cerebral protective effect, or cause hyperperfusion, however the mechanism is unclear. Pterygopalatine ganglion (PPG) is a parasympathetic ganglion that innervates cerebral blood vessels. Stimulation of PPG increased cerebral blood flow. We found for the first time that isoflurane, a general anesthetic, can directly activatesPPG. Choline receptors expressed by PPG are known to be predominantly nAchR, while isoflurane can bind to nAchR transmembrane sites. Studies have shown that the vasodilation effect of isoflurane is NO dependent, while PPG contains a large amount of neuronal NO synthase. Therefore, we postulate that isoflurane can release vasodilator such as NO by activating nAchR in PPG. Vasodilatory effects of isoflurane have been reported with a big variation in diabetic patients. We found that the expression of neuronal NO synthase was inconsistent in PPG of diabetic mice at different stages. It is speculated that this is the main reason for different vasodilatory effects of isoflurane. In this study, we will apply genetic and neurobiological studies to elucidate the characteristics of the NO release isoflurane through nAchR activation. We will also analysis how the changes of transcriptome in diabetic PPGs at different stages affect the isoflurane-induced vasodilatory. Our study will provide a theoretical basis for regulating isoflurane-induced cerebral vasodilation and optimizing the anesthesia management for diabetic patients.