大脑动脉血管周围交感神经的中断可提供针对缺血的神经保护作用。
Interruption of perivascular sympathetic nerves of cerebral arteries offers neuroprotection against ischemia.
作者信息
Lee Reggie H, Couto E Silva Alexandre, Lerner Francesca M, Wilkins Carl S, Valido Stephen E, Klein Daniel D, Wu Celeste Y, Neumann Jake T, Della-Morte David, Koslow Stephen H, Minagar Alireza, Lin Hung Wen
机构信息
Cerebral Vascular Disease Laboratories, University of Miami Miller School of Medicine, Miami, Florida.
Department of Neurology, University of Miami Miller School of Medicine, Miami, Florida.
出版信息
Am J Physiol Heart Circ Physiol. 2017 Jan 1;312(1):H182-H188. doi: 10.1152/ajpheart.00482.2016. Epub 2016 Nov 18.
UNLABELLED
Sympathetic nervous system activity is increased after cardiopulmonary arrest, resulting in vasoconstrictor release from the perivascular sympathetic nerves of cerebral arteries. However, the pathophysiological function of the perivascular sympathetic nerves in the ischemic brain remains unclear. A rat model of global cerebral ischemia (asphyxial cardiac arrest, ACA) was used to investigate perivascular sympathetic nerves of cerebral arteries via bilateral decentralization (preganglionic lesion) of the superior cervical ganglion (SCG). Decentralization of the SCG 5 days before ACA alleviated hypoperfusion and afforded hippocampal neuroprotection and improved functional outcomes. These studies can provide further insights into the functional mechanism(s) of the sympathetic nervous system during ischemia.
NEW & NOTEWORTHY: Interruption of the perivascular sympathetic nerves can alleviate CA-induced hypoperfusion and neuronal cell death in the CA1 region of the hippocampus to enhance functional learning and memory.
未标记
心肺骤停后交感神经系统活动增加，导致脑动脉血管周围交感神经释放血管收缩剂。然而，血管周围交感神经在缺血性脑内的病理生理功能仍不清楚。采用全脑缺血大鼠模型（窒息性心脏骤停，ACA），通过双侧颈上神经节（SCG）去传入（节前损伤）来研究脑动脉的血管周围交感神经。在ACA前5天对SCG进行去传入可减轻灌注不足，提供海马神经保护并改善功能结局。这些研究可为缺血期间交感神经系统的功能机制提供进一步的见解。
新进展与值得注意之处
血管周围交感神经的中断可减轻心脏骤停引起的灌注不足以及海马CA1区的神经元细胞死亡，从而增强功能性学习和记忆。
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