Kotani N, Hashimoto H, Sessler D I, Yatsu Y, Muraoka M, Matsuki A
Department of Anesthesiology, University of Hirosaki, Japan.
Anesthesiology. 1999 Dec;91(6):1823-33. doi: 10.1097/00000542-199912000-00037.
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.
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.
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.
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.
吸烟会改变肺泡巨噬细胞的多种功能，是术后肺部并发症的重要危险因素。因此，作者检验了以下假设：在氟烷和异氟烷麻醉并机械通气期间，接触烟雾会损害肺泡巨噬细胞的抗菌和促炎反应。
30只对照大鼠和30只接触香烟烟雾的大鼠用1.5倍最低肺泡浓度的氟烷和异氟烷进行机械通气。将10只接触烟雾的动物和10只对照动物分配到三种不同的麻醉时长（0、2和6小时）之一。测定聚集细胞的比例和细胞分布。测量调理吞噬和非调理吞噬作用。将杀菌活性确定为杀死单核细胞增生李斯特菌的能力。通过半定量逆转录聚合酶链反应测量白细胞介素（IL）-1α、IL-1β、IL-6、巨噬细胞炎性蛋白-2、干扰素-γ和肿瘤坏死因子-α的表达。通过酶联免疫吸附测定法测量这些细胞因子的肺灌洗浓度。
在氟烷和异氟烷麻醉期间，两组中聚集巨噬细胞的比例均增加，而非调理和调理吞噬作用以及杀菌活性随时间显著降低。接触烟雾的大鼠中观察到的反应几乎是对照大鼠中观察到的反应的两倍。除IL-6外，所有促炎细胞因子的基因表达和产生在麻醉期间增加了2至20倍。对照大鼠中IL-1β、干扰素-γ和肿瘤坏死因子-α的增加比接触烟雾的大鼠中的增加大1.5至8倍。
麻醉期间肺泡巨噬细胞的抗菌和促炎反应受到烟雾暴露的显著抑制。我们的数据表明，烟雾暴露会降低麻醉期间免疫防御的功效。
