Cervin A, Lindberg S, Mercke U
Department of Oto-Rhino-Laryngology, University Hospital, Lund, Sweden.
Otolaryngol Head Neck Surg. 1995 Jun;112(6):714-22. doi: 10.1016/S0194-59989570181-8.
The effect of halothane on mucociliary activity in the rabbit maxillary sinus in vivo was recorded photoelectrically. Administration of halothane (1%, 2% or 4%) into the maxillary sinus induced a temporary acceleration of mucociliary activity. The peak increase (39.1% +/- 9.1%, p < 0.05, n = 5) was seen after the 4% concentration. Long-term exposure (60 minutes) of the maxillary sinus to halothane (2%) first induced an increase of 28.4% +/- 4.6% (p < 0.05, n = 6), lasting approximately four minutes, and followed after about 15 minutes by a decrease of mucociliary activity. The maximum decrease during the 60-minute period was 19.6% +/- 2.8% (p < 0.05, n = 6). Mucociliary activity returned to its baseline level approximately 25 minutes after withdrawal of halothane. Halothane delivered to the rabbit through a tracheal cannula at 1.1% for 60 minutes did not impair mucociliary activity in the maxillary sinus. On the contrary, it initially stimulated mucociliary activity, 19.9% +/- 2.7% (p < 0.05, n = 5). There was also an initial increase in respiratory rate from 62 +/- 7.3 to 89 +/- 12.9 breaths per minute (p < 0.05), which was noticeable after approximately 10 seconds and lasted 4 to 5 minutes. The dose-dependent increase in mucociliary activity seen after short-term exposure to halothane is probably due to stimulation of afferent C fibers, because halothane may be considered an airway irritant. The reversible depressant effect seen after 15 minutes of exposure is in accordance with findings in previous studies in vitro. The mechanism by which halothane impairs mucociliary activity is at present not known. However, halothane administered to the lower airways does not impair mucociliary activity in the maxillary sinus, indicating that halothane affects the ciliated epithelium directly and that the state of anesthesia itself has no effect on mucociliary activity.
采用光电记录法研究了氟烷对兔上颌窦体内黏液纤毛活性的影响。向上颌窦内注入1%、2%或4%的氟烷会引起黏液纤毛活性暂时加快。4%浓度的氟烷注入后，黏液纤毛活性达到峰值增加（39.1%±9.1%，p<0.05，n = 5）。上颌窦长期暴露于2%氟烷（60分钟），首先引起28.4%±4.6%的增加（p<0.05，n = 6），持续约4分钟，随后约15分钟后黏液纤毛活性下降。60分钟内最大下降幅度为19.6%±2.8%（p<0.05，n = 6）。停止使用氟烷后约25分钟，黏液纤毛活性恢复至基线水平。通过气管插管以1.1%的浓度给兔输入氟烷60分钟，未损害上颌窦的黏液纤毛活性。相反，它最初刺激了黏液纤毛活性，增加了19.9%±2.7%（p<0.05，n = 5）。呼吸频率也最初从每分钟62±7.3次增加到89±12.9次（p<0.05），大约10秒后明显可见，持续4至5分钟。短期接触氟烷后出现的黏液纤毛活性剂量依赖性增加可能是由于传入C纤维受到刺激，因为氟烷可被视为气道刺激物。接触15分钟后出现的可逆性抑制作用与先前体外研究结果一致。目前尚不清楚氟烷损害黏液纤毛活性的机制。然而，向下呼吸道给药的氟烷不会损害上颌窦的黏液纤毛活性，这表明氟烷直接影响纤毛上皮，且麻醉状态本身对黏液纤毛活性没有影响。
