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气体栓塞与基于表面活性剂的干预措施:对长期太空活动的影响

Gas embolism and surfactant-based intervention: implications for long-duration space-based activity.

作者信息

Eckmann David M, Zhang Jie, Lampe Joshua, Ayyaswamy Portonovo S

机构信息

Department of Anesthesiology and Critical Care, University of Pennsylvania, Philadelphia, PA 19104, USA.

出版信息

Ann N Y Acad Sci. 2006 Sep;1077:256-69. doi: 10.1196/annals.1362.039.

Abstract

Intravascular gas embolism can occur with decompression in space flight, and it commonly occurs during cardiac and vascular surgery. Intravascular bubbles may be deposited into any end organ such as the heart or the brain. Surface interactions between the bubble and the endothelial cells lining the vasculature result in serious impairment of blood flow and can lead to heart attack, stroke, or even death. Surfactant-based intervention is a novel treatment for gas embolism. Intravascular surfactant can adsorb onto the gas-liquid interface and compete with blood-borne macromolecules for interfacial occupancy. Surfactants can retard the progress of pathophysiological molecular and cellular events stimulated by the bubble surface, including endothelial cell injury and initiation of blood clotting. Bulk and surface transport of a surfactant to provide competition for interfacial occupancy is a therapeutic strategy because surfactant adsorption can dominate protein (or other macromolecule) adsorption. The presence of surfactant along the gas-liquid interface also induces variation in the interfacial tension, which in turn affects the blood flow and the bubble motion. We describe the interplay between biological transport processes and physiological events occurring and the cellular and molecular level in vascular gas embolization. Special consideration is given to modeling the transport and hydrodynamic interactions associated with surfactant-based intervention.

摘要

血管内气体栓塞可发生于太空飞行减压过程中,也常见于心脏和血管手术期间。血管内气泡可能沉积于任何终末器官,如心脏或大脑。气泡与血管系统内衬的内皮细胞之间的表面相互作用会导致血流严重受损,并可能引发心脏病发作、中风甚至死亡。基于表面活性剂的干预是一种治疗气体栓塞的新方法。血管内表面活性剂可吸附于气液界面,并与血液中的大分子竞争界面占据。表面活性剂可延缓由气泡表面刺激引发的病理生理分子和细胞事件的进展,包括内皮细胞损伤和凝血启动。通过表面活性剂的大量和表面转运以提供界面占据竞争是一种治疗策略,因为表面活性剂吸附可主导蛋白质(或其他大分子)吸附。气液界面处表面活性剂的存在还会引起界面张力变化,进而影响血流和气泡运动。我们描述了血管气体栓塞过程中生物转运过程与发生在细胞和分子水平的生理事件之间的相互作用。特别关注基于表面活性剂干预的转运和流体动力学相互作用建模。

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