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Exposure to cigarette smoke impairs alveolar macrophage functions during halothane and isoflurane anesthesia in rats
N Kotani1, H Hashimoto, D I Sessler
1Department of Anesthesiology, University of Hirosaki, Japan. nao@cc.hirosaki-u.ac.jp
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 Listeria monocytogenes. The expression of interleukin (IL)-1alpha, IL-1beta, 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-1beta, interferon-gamma, and tumor necrosis factor-alpha 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.
Insights
Cigarette smoke exposure significantly impairs alveolar macrophage immune defenses during anesthesia, reducing their ability to fight infections. This suggests smoke exposure compromises immune responses crucial for recovery from surgery.
Area of Science:
- Anesthesiology
- Immunology
- Pulmonary Medicine
Background:
- Smoking is a known risk factor for postoperative pulmonary complications.
- Alveolar macrophages play a critical role in lung immunity.
- Anesthesia and mechanical ventilation can impact immune function.
Purpose of the Study:
- To investigate the effects of smoke exposure on alveolar macrophage function during halothane and isoflurane anesthesia.
- To test the hypothesis that smoke exposure impairs antimicrobial and proinflammatory responses.
Main Methods:
- Rats exposed to cigarette smoke were mechanically ventilated with halothane and isoflurane.
- Phagocytosis, microbicidal activity, and cytokine gene expression/production were measured.
- Cytokine levels in pulmonary lavage fluid were quantified.
Main Results:
- Smoke exposure significantly decreased phagocytosis and microbicidal activity in alveolar macrophages.
- Proinflammatory cytokine expression and production increased during anesthesia, but less so in smoke-exposed rats.
- Smoke-exposed rats showed approximately double the impairment in immune responses compared to controls.
Conclusions:
- Smoke exposure markedly suppresses antimicrobial and proinflammatory responses of alveolar macrophages during anesthesia.
- These findings indicate that smoking reduces the effectiveness of immune defenses during the perioperative period.
- Alveolar macrophage dysfunction due to smoking may contribute to increased postoperative pulmonary complications.