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许多研究发现,神经肽与脑血管疾病密切相关,但神经肽Y(NPY)P物质(SP)在脑血管疾病中的意义尚未明了,缺血脑组织内单胺类递质的变化仍有争议.实验用健康猕猴6只,体重2.5～5公斤.在左侧大脑顶额叶交界区,采用开窗式局部脑缺血模型制成1.5×1.5cm~2的局部缺血灶,分别在缺血 2～4小时及24～48小时后取材,用免疫组化ABC法观察NPY、SP、多巴胺-β-羟化酶(DBH)在不同缺血期的改变.用与缺血区相对应的右侧顶额叶大脑皮质作对照.结果发现,缺血2～4小时后,SP阳性纤维在缺血区的分布较对照组明显增多,有显著性差异(P<0.01),阳性胞体与对照组无明显差别,均较稀少;NPY及DBH阳性纤维及胞体与对照组相似.局部缺血持续24～48小时后,SP阳性纤维持续增多,NPY及DBH阳性纤维则明显减少,有显著性差异(P<0.01),部分NPY阳性胞体变形,脱体边界不清,突起不明显.以上结果提示,在缺血过程,SP合成及释放增加可能与参与抗损伤及修复、改善血循环有关;NPY的降低,可能与机体的反馈抑制及神经元受损、功能降低有关;缺血初期,DBH仍可通过脑内α受体参与脑血管扩张调节,但缺血后期明显降低则可能是神经元受损,合成功能下降之故.
Many studies have found that neuropeptides and cerebrovascular disease are closely related, but the significance of neuropeptide Y (NPY) substance P (SP) in cerebrovascular disease is not yet clear, changes in monoamine neurotransmitters in ischemic brain tissue is still controversial Six healthy experimental monkeys (2.5-5 kg body weight) were used in this study.The ischemic foci of 1.5 × 1.5cm ~ 2 were made by using the window-opening local cerebral ischemia model at the border of the frontal lobe of the left cerebrum, Blood samples were taken from 2 to 4 hours and from 24 to 48 hours after the ischemia, and the changes of NPY, SP and dopamine-β-hydroxylase (DBH) in different ischemic periods were observed by immunohistochemical ABC method. Right frontal cortex cerebral cortex as a control and found that 2 to 4 hours after ischemia, SP positive fibers in the ischemic area was significantly increased compared with the control group, a significant difference (P <0.01), positive cell bodies and control Group, there were no significant differences between the two groups, all of which were more scarce.NFY and DBH positive fibers and cell bodies were similar to the control group.When the ischemia continued for 24-48 hours, the number of SP positive fibers and the number of positive NPY and DBH fibers decreased significantly (P <0.01), some of the NPY positive cell body deformity, off-body boundary is unclear, the protrusion is not obvious.The above results suggest that in the ischemic process, SP Increased release may be involved in the anti-injury and repair, improve blood circulation; NPY decreased, may be related to the body’s feedback inhibition and neuronal damage, decreased function; early ischemic, DBH can still be involved in α receptors through the brain Cerebrovascular dilatation regulation, but significantly decreased late ischemic may be neuronal damage, decreased synthesis function.