Exposure to cigarette smoke impairs alveolar macrophage functions during halothane and isoflurane anesthesia in rats

被引:22
作者
Kotani, N [1 ]
Hashimoto, H
Sessler, DI
Yatsu, Y
Muraoka, M
Matsuki, A
机构
[1] Hirosaki Univ, Sch Med, Dept Anesthesiol, Outcomes ResTM Grp, Hirosaki, Aomori 0368562, Japan
[2] Univ Calif San Francisco, Dept Anesthesia & Perioperat Care, San Francisco, CA 94143 USA
[3] Ludwig Boltzmann Inst Clin Anesthesia & Intens Ca, Vienna, Austria
[4] Univ Vienna, Dept Anesthesia & Gen Intens Care, Vienna, Austria
关键词
immune response; mechanical ventilation; smoking; volatile anesthetic;
D O I
10.1097/00000542-199912000-00037
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Background: Smoking alters numerous alveolar macrophage functions and is an important risk factor for postoperative pulmonary complications. The authors therefore tested the hypothesis that smoke exposure impairs antimicrobial and proinflammatory responses in alveolar macrophages during halothane and isoflurane anesthesia with mechanical ventilation. Methods: Thirty control rats and 30 rats exposed to cigarette smoke were mechanically ventilated with 1.5 minimum alveolar concentration halothane and isoflurane. Ten smoke-exposed and control animals were assigned to one of three different anesthetic durations (0, 2, and 6 h). The fraction of aggregated cells and cell distribution were determined. Opsonized and unopsonized phagocytosis was measured. Microbicidal activity was determined as the ability to kill Lister in monocytogenes. The expression of interleukin (IL)-1 alpha, IL-1 beta, IL-6, macrophage inflammatory protein-2, interferon-gamma, and tumor necrosis factor-alpha was measured by semiquantitative reverse-transcription polymerase chain reaction. Pulmonary lavage concentrations of these cytokines were measured by enzyme-linked immunosorbent assay. Results: During both halothane and isoflurane anesthesia, the fraction of aggregated macrophages increased, whereas unopsonized and opsonized phagocytosis and microbicidal activity decreased significantly over time in both groups. Responses observed in smoke-exposed rats were almost twice as great as those observed in the control rats. Gene expression and production of all proinflammatory cytokines except IL-6 increased 2-20-fold during anesthesia. The increases in IL-1 beta, interferon-gamma, and tumor necrosis factor-cu in the control rats were 1.5-8 times greater than those in the smoke-exposed rats. Conclusion: Antimicrobial and proinflammatory responses of alveolar macrophages during anesthesia were markedly suppressed by smoke exposure. Our data suggest that smoke exposure reduces the efficacy of immune defenses during anesthesia.
引用
收藏
页码:1823 / 1833
页数:11
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