Morris David G, Sheppard Dean
Respiratory Research, Roche Palo Alto, LLC, F. Hoffman-LaRoche, Ltd., Palo Alto.
Physiology (Bethesda). 2006 Dec;21:396-403. doi: 10.1152/physiol.00027.2006.
Pulmonary emphysema results from the loss of intricate alveolar architecture and progressive simplification of small and highly effective gas-exchanging units into large, inefficient cyst-like spaces. Because of the loss of alveolar gas-exchanging units and the capillary bed within them, blood oxygen levels eventually fall and pressures within the pulmonary circulation rise. Recent insights from genetically manipulated mouse models have refined our understanding of the molecular events that prevent or promote the development of pulmonary emphysema. Capitalizing on an improved molecular understanding of emphysema with improved therapeutics has the potential to enhance both the survival and quality of life of patients with this common lung disease.
肺气肿是由于复杂的肺泡结构丧失，以及小而高效的气体交换单位逐渐简化为大的、低效的囊状空间所致。由于肺泡气体交换单位及其内毛细血管床的丧失，血氧水平最终会下降，肺循环压力会升高。最近对基因操作小鼠模型的深入研究，使我们对预防或促进肺气肿发展的分子事件有了更深入的了解。利用对肺气肿分子机制的深入理解开发更好的治疗方法，有可能提高这种常见肺部疾病患者的生存率和生活质量。
