Foronjy Robert F, Mercer Becky A, Maxfield Mark W, Powell Charles A, D'Armiento Jeanine, Okada Yasunori
Department of Medicine, Division of Molecular Medicine and Pulmonary Medicine, Columbia University, New York, USA.
Exp Lung Res. 2005 Jul-Aug;31(6):547-62. doi: 10.1080/019021490951522.
The murine smoke-induced model produces histologic emphysema. The authors sought to assess whether the structural emphysema that occurred correlated with the development of compliance changes. The study exposed 2 strains of mice (CBA/J/J x C57BL/6J and A/J) to chronic cigarette smoke. Lung compliance and morphometry were measured. The smoking model generated significant emphysema in A/J mice in the absence of changes in compliance, lung matrix, or apoptosis. Importantly, there was no correlation between the emphysema measured by lung morphometry and pulmonary compliance. This lack of correlation suggests that the mechanisms involved in anatomic emphysema may be distinct from those that cause the loss of elastic recoil.
小鼠烟雾诱导模型会产生组织学上的肺气肿。作者试图评估所发生的结构性肺气肿是否与顺应性变化的发展相关。该研究将2种品系的小鼠（CBA/J/J×C57BL/6J和A/J）暴露于慢性香烟烟雾中。测量了肺顺应性和形态学指标。吸烟模型在A/J小鼠中产生了显著的肺气肿，而顺应性、肺基质或细胞凋亡均未发生变化。重要的是，通过肺形态学测量的肺气肿与肺顺应性之间没有相关性。这种缺乏相关性表明，解剖性肺气肿所涉及的机制可能与导致弹性回缩丧失的机制不同。
