首页> 外文会议>Aachen Symposium on Natural and Artificial Respiration >Cell Physiology and Fluid Mechanics in the Pulmonary Alveolus and Its Capillaries
【24h】

Cell Physiology and Fluid Mechanics in the Pulmonary Alveolus and Its Capillaries

机译:肺部肺泡及其毛细管的细胞生理学和流体力学

获取原文

摘要

Depending on the applied ventilation strategy, mechanical ventilation leads to alveolar epithelial and capillary endothelial damage. Protective ventilatory approaches try to minimize this biotrauma while still ensuring sufficient gas exchange. However, the optimization of ventilation strategies is hampered by the lack of insights into the cellular and molecular mechanisms underlying ventilator-induced lung injury, and by the lack of morphological and biomechanical information pertinent to the development of suitable computational and experimental models for ventilation-dependent biofluid mechanics [13, 15, 30]. Here, we present our experimental and simulation studies at the level of the alveoli and their capillaries. Regarding capillary perfusion, we show the results concerning the mechanisms of hypoxic pulmonary vasoconstriction as well as an enlarged experimental model for studying the flow in pulmonary capillary networks. We studied alveolar mechanics, both in the mouse model and in a simulation model, providing insights into the effects of ventilation strategies with regard to the underlying lung injury and disease. Further, we present our results concerning the role of the mechanosensitive transient receptor potential channel TRPV4.
机译:根据应用的通风策略,机械通风导致肺泡上皮和毛细管内皮损伤。保护通气方法尽量减少这种生物造影,同时仍然确保足够的气体交换。然而,通风策略的优化受到呼吸机诱导的肺损伤的细胞和分子机制缺乏见解,并且通过缺乏与开发适用于通风依赖性的计算和实验模型的形态和生物力学信息生物流体力学[13,15,30]。在这里,我们在肺泡和毛细血管的水平上展示了我们的实验和模拟研究。关于毛细血管灌注,我们展示了关于缺氧肺血管混凝机制的结果以及研究肺毛细管网络流量的扩大实验模型。我们研究了小鼠模型和仿真模型中的肺泡力学,既是仿真模型,介绍了通风策略对潜在肺损伤和疾病的影响。此外,我们提出了关于机械静脉受体受体电位通道TRPV4的作用的结果。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号