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Mechanisms involved in the cerebrovascular dilator effects of cortical spreading depression.
Progress in Neurobiology ( IF 6.7 ) Pub Date : 2008-10-07 , DOI: 10.1016/j.pneurobio.2008.09.008
David W Busija 1 , Ferenc Bari , Ferenc Domoki , Takashi Horiguchi , Katsuyoshi Shimizu
Affiliation  

Cortical spreading depression (CSD) leads to dramatic changes in cerebral hemodynamics. However, mechanisms involved in promoting and counteracting cerebral vasodilator responses are unclear. Here we review the development and current status of this important field of research especially with respect to the role of perivascular nerves and nitric oxide (NO). It appears that neurotransmitters released from the sensory and the parasympathetic nerves associated with cerebral arteries, and NO released from perivascular nerves and/or parenchyma, promote cerebral hyperemia during CSD. However, the relative contributions of each of these factors vary according to species studied. Related to CSD, axonal and reflex responses involving trigeminal afferents on the pial surface lead to increased blood flow and inflammation of the overlying dura mater. Counteracting the cerebral vascular dilation is the production and release of constrictor prostaglandins, at least in some species, and other possibly yet unknown agents from the vascular wall. The cerebral blood flow response in healthy human cortex has not been determined, and thus it is unclear whether the cerebral oligemia associated with migraines represents the normal physiological response to a CSD-like event or represents a pathological response. In addition to promoting cerebral hyperemia, NO produced during CSD appears to initiate signaling events which lead to protection of the brain against subsequent ischemic insults. In summary, the cerebrovascular response to CSD involves multiple dilator and constrictor factors produced and released by diverse cells within the neurovascular unit, with the contribution of each of these factors varying according to the species examined.

中文翻译:

脑血管扩张皮层扩散抑制作用的机制。

皮质扩散抑制(CSD)导致大脑血流动力学的急剧变化。但是,促进和抵消脑血管舒张反应的机制尚不清楚。在这里,我们回顾这一重要研究领域的发展和现状,尤其是关于血管周围神经和一氧化氮(NO)的作用。似乎从与脑动脉相关的感觉神经和副交感神经释放的神经递质以及从血管周围神经和/或实质释放的NO促进了CSD期间的脑充血。但是,这些因素各自的相对贡献因所研究的物种而异。与CSD相关,涉及三叉神经传入神经膜的轴突和反射反应导致血液流量增加和上硬脑膜发炎。至少在某些物种中,收缩性前列腺素的产生和释放与脑血管的扩张相抵消,而血管壁中的其他可能还未知的因子会产生抑制作用。尚未确定健康人皮层中的脑血流反应,因此尚不清楚与偏头痛相关的脑性低尿症是代表对CSD样事件的正常生理反应还是代表病理反应。除了促进脑充血,在CSD期间产生的NO似乎会引发信号传导事件,从而保护大脑免受随后的缺血性损伤。总之,脑血管对CSD的反应涉及神经血管单位内各种细胞产生和释放的多种扩张器和收缩器因子,
更新日期:2019-11-01
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