Ghadiali Samir, Huang Y
Department of Biomedical Engineering, The Ohio State University, Columbus, Ohio 43221, USA.
Crit Rev Biomed Eng. 2011;39(4):297-317. doi: 10.1615/critrevbiomedeng.v39.i4.40.
The mechanical forces generated during the ventilation of patients with acute lung injury causes significant lung damage and inflammation. Low-volume ventilation protocols are commonly used to prevent stretch-related injury that occurs at high lung volumes. However, the cyclic closure and reopening of pulmonary airways at low lung volumes, i.e., derecruitment and recruitment, also causes significant lung damage and inflammation. In this review, we provide an overview of how biomedical engineering techniques are being used to elucidate the complex physiological and biomechanical mechanisms responsible for cellular injury during recruitment/derecruitment. We focus on the development of multiscale, multiphysics computational models of cell deformation and injury during airway reopening. These models, and the corresponding in vitro experiments, have been used to both elucidate the basic mechanisms responsible for recruitment/derecruitment injury and to develop alternative therapies that make the epithelium more resistant to injury. For example, models and experiments indicate that fluidization of the cytoskeleton is cytoprotective and that changes in cytoskeletal structure and cell mechanics can be used to mitigate the mechanotransduction of oscillatory pressure into inflammatory signaling. The continued application of biomedical engineering techniques to the problem of recruitment/derecruitment injury may therefore lead to novel and more effective therapies.
急性肺损伤患者通气过程中产生的机械力会导致严重的肺损伤和炎症。小潮气量通气方案通常用于预防高肺容积时发生的牵张相关损伤。然而，在低肺容积时肺气道的周期性关闭和重新开放，即肺不张和复张，也会导致严重的肺损伤和炎症。在本综述中，我们概述了生物医学工程技术如何用于阐明在肺复张/肺不张期间导致细胞损伤的复杂生理和生物力学机制。我们重点关注气道重新开放过程中细胞变形和损伤的多尺度、多物理场计算模型的开发。这些模型以及相应的体外实验，已被用于阐明肺复张/肺不张损伤的基本机制，并开发使上皮细胞更耐受损伤的替代疗法。例如，模型和实验表明细胞骨架的流化具有细胞保护作用，并且细胞骨架结构和细胞力学的变化可用于减轻振荡压力向炎症信号的机械转导。因此，生物医学工程技术持续应用于肺复张/肺不张损伤问题可能会带来新的、更有效的治疗方法。
