在用黄素预治疗后的肺血栓栓塞的实验模型中的肺微循环
V I Evlakhov1, I Z Poyasov2, T P Berezina2
1Laboratory of Visceral System Physiology, Institute of Experimental Medicine, St. Petersburg, Russia. viespbru@mail.ru.
Bulletin of experimental biology and medicine
|August 10, 2023
概括
黄素预治疗在栓塞过程中降低了肺血管抵抗力,这表明它阻断了L型和T型通道,并激活了KATP通道,影响了肺循环.
科学领域:
- 药理学 药理学是指药理学的学科.
- 心血管生理学心血管生理学
- 肺部医学 肺部医学
背景情况:
- 肺动脉栓塞 (PAE) 导致肺微循环发生显著变化.
- 了解PAE诱导的血管抵抗背后的机制对于开发有效的治疗方法至关重要.
- 通道和KATP通道在调节血管度方面发挥着关键作用.
研究的目的:
- 调查诺基因在PAE期间对肺微循环的影响.
- 确定克洛洛奎因在肺血管系统中的作用背后的特定离子通道机制.
主要方法:
- 隔离的 perfused 子肺部模型.
- 肺动脉栓塞是诱导的.
- 测量了血液动力学参数,包括肺血管阻力,毛细血管前后阻力和毛细血管过系数.
- 克洛洛昆的作用与米贝弗拉迪尔 (T型Ca2+通道阻塞剂) 和尼菲迪平 (L型Ca2+通道阻塞剂) 相比较.
- 评估了诺基因和 Glibenclamide (KATP通道阻断剂) 的联合作用.
主要成果:
- 与对照组相比,黄素预治疗显著减轻了肺血管抵抗和毛细血管前后抵抗的增加.
- 叶绿素的作用比单独服用米贝弗拉迪尔或尼菲迪平的效果要弱.
- 毛细血管过系数的变化与毛细血管前阻力变化相关.
- 结合诺基因和草甘胺的预处理模仿了尼菲迪平的作用,表明诺基因激活了KATP通道.
结论:
- 氨酸表现出L型和T型通道阻断剂的特性.
- 氨酸作为肺血管中的KATP通道的激活剂.
- 这些联合作用有助于克洛洛昆对PAE诱导的血液动力学变化的保护作用.
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