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Gastrointestinal Motility Monitor GIMM
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脑卒中改变肠道神经元的功能,损害了光滑肌肉的放松,并破坏了肠道过境的调节
Kathryn Prame Kumar1, Jenny L Wilson1, Huynh Nguyen1
1Centre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences at Monash Health, Monash Medical Centre Monash University Clayton Victoria Australia.
Journal of the American Heart Association
|January 23, 2024
概括
卒中通过激活交感神经系统来破坏肠道运动,减少肠道神经元中的氧化合成酶. 这会损害光滑肌肉的放松,并减缓肠道通道.
科学领域:
- 神经胃肠病学 神经胃肠病学
- 卒中病理生理学 卒中病理生理学
- 免疫学 免疫学 免疫学
背景情况:
- 缺血性中风后,肠道动力障碍经常发生,但其潜在机制尚不清楚.
- 肠道神经系统调节肠道运动,最近的证据表明巨细胞相互作用.
- 目前尚不清楚中风是否直接通过肠道神经系统或间接通过炎症性巨细胞影响肠道运动.
研究的目的:
- 为了研究中风后肠道动力障碍的机制.
- 确定肠道神经系统和巨细胞在中风引起的肠道功能障碍中的作用.
主要方法:
- 在小鼠中使用了永久性内脑中动脉阻塞模型的中风.
- 在中风后24小时进行了体内和体外肠道运动性测定,流动细胞计,免疫光和转录组分析.
- 使用6-氧多巴胺进行化学同情切除术.
主要成果:
- 脑卒中引起的肠动性,其特点是肌肉巨细胞的招募和重新分配,远离肌肠.
- 脑卒中后的肌肠神经元表现出神经元氧化合成酶 (nNOS) 表达的减少,与增强的肠直肌收缩相关.
- 化学交感切除术预防了nNOS损失和肠道通行正常化,表明交感神经系统的参与.
结论:
- 脑卒中后的交感神经系统激活有助于肠道不运动.
- 肌肠神经元中的nNOS表达减少会损害光滑肌肉的放松,并扰乱肠道通道.
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