A MODEL OF PULMONARY ATELECTASIS IN RATS - ACTIVATION OF ALVEOLAR MACROPHAGE AND CYTOKINE RELEASE

被引:40
作者
KISALA, JM
AYALA, A
STEPHAN, RN
CHAUDRY, IH
机构
[1] MICHIGAN STATE UNIV,DEPT PHYSIOL,E LANSING,MI 48824
[2] SUNY BUFFALO,DEPT SURG,BUFFALO,NY 14215
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1993年 / 264卷 / 03期
关键词
INTERLEUKIN-1; TUMOR NECROSIS FACTOR; ALVEOLAR MACROPHAGES; ATELECTASIS;
D O I
10.1152/ajpregu.1993.264.3.R610
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Although atelectasis frequently occurs after surgery and trauma, and such patients have elevated body temperatures, the mechanism of temperature elevation secondary to atelectasis is unknown. Moreover, a small animal model has not been available to study the pathophysiology of pulmonary atelectasis. The purpose of this study, therefore, was to develop a model of pulmonary atelectasis in rats. Because interleukin-1 (IL-1) and tumor necrosis factor (TNF), both potent pyrogens, are produced by macrophages during infection and inflammation, our aim was also to determine whether alveolar macrophages produce IL-1 or TNF in response to atelectasis. Whole-lung atelectasis was produced in rats by ligating the left main stem bronchus while maintaining ventilation of the right lung. After a 1-h period of atelectasis, alveolar macrophages were harvested from the right and left lungs and incubated for 24 h, and the supernatants were assayed for IL-1 and TNF. Both IL-1 and TNF levels of macrophage cultures from the atelectatic lung were significantly increased compared with the control lung. These results suggest that increased IL-1 or TNF production by alveolar macrophages may be responsible for fever caused by atelectasis.
引用
收藏
页码:R610 / R614
页数:5
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