由挥发性麻醉剂诱导的年龄相关的大脑血管扩张是由NG2+血管壁细胞介导的
Hang Zhou1,2, Viola Neudecker1, Jose F Perez-Zoghbi1
1Department of Anesthesiology, Columbia University Irving Medical Center, New York, NY, 100032, USA.
Communications biology
|November 15, 2024
概括
挥发性麻醉剂,如sevoflurane和isoflurane,通过影响NG2+血管壁细胞,在成年小鼠中引起大脑血管扩张. 这种效应在年轻小鼠中不那么明显,突出了年龄相关的机制.
科学领域:
- 神经科学是一个神经科学.
- 麻醉学 麻醉学
- 血管生物学 血管生物学
背景情况:
- 麻醉通过改变大脑血管直径来影响大脑血液流动.
- 挥发性麻醉剂是常用的,但它们对大脑血管系统的确切影响,尤其是发育中的大脑,需要进一步阐明.
研究的目的:
- 调查sevoflurane和isoflurane对不同年龄组小鼠的大脑动脉小和毛细血管直径的影响.
- 确定麻醉诱导的大脑血管扩张的细胞机制,重点关注NG2+血管壁细胞及其在年龄依赖反应中的作用.
主要方法:
- 在活体中使用双光子成像来可视化和测量在麻醉下年轻和成年小鼠的大脑血管直径.
- 评估了NG2+血管壁细胞中的细胞质水平.
- 使用光遗传学操纵和细胞剥离技术来确定NG2+血管壁画细胞的功能作用.
- 在未成熟的大脑中分析了Kir6.1的表达水平,这是对ATP敏感通道的子单元.
主要成果:
- 在成年小鼠中,sevoflurane和isoflurane诱导皮质动脉小动脉和毛细血管的显著扩张,在幼鼠中影响减弱,在婴儿中没有观察到扩张.
- 麻醉诱导的血管扩张与NG2+血管壁细胞中细胞质水平降低相关.
- 光遗传激活/抑制NG2+血管壁细胞调节血管直径,并且它们的切除取消了麻醉诱导的血管扩张.
- 不成熟的大脑显示较少的NG2+壁细胞和较低的Kir6.1表达,与减少的血管扩张反应相关.
结论:
- NG2+血管壁细胞是麻醉诱导的大脑血管扩张的关键调解者.
- 血管扩张的年龄差异与NG2+壁细胞的数量和功能有关,特别是它们的Kir6.1.1.表达.
- 这些发现为控制麻醉药在不同发育阶段对大脑的影响的神经血管机制提供了新的见解.
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