Knight P R, Nahrwold M L, Bedows E
Antimicrob Agents Chemother. 1981 Sep;20(3):298-306. doi: 10.1128/AAC.20.3.298.
Replication of measles virus in BSC cells was studied in the presence of enflurane (2-chloro-1,1,2-trifluoroethyl difluoromethyl ether), a commonly used volatile anesthetic agent, and its isomer, isoflurane (1-chloro-2,2,2-trifluoroethyl difluoromethyl ether). At clinical concentrations of the anesthetics (up to 4%), cell division was retarded, whereas only minimal toxic cellular effects were observed. The appearance of progeny virus from the cell cultures exposed to these anesthetics was decreased in a dose-related manner. Incorporation of [(3)H]uridine into measles virus nucleocapsids also decreased progressively with increasing anesthetic concentrations. In comparing the inhibition of measles virus replication in the presence of halothane (2-bromo-2-chloro,1,1,1-trifluoroethane), enflurane, or isoflurane, it was found that both inhibition of the appearance of infectious virus at 48 h postinfection and incorporation of [(3)H]uridine into measles virus nucleocapsids were proportional to the anesthetic concentrations. An equivalent degree of effect was produced by anesthetically equivalent concentrations of the three anesthetics (minimal alveolar concentration) but not by absolute concentrations. In addition, recovery of infectious virus synthesis from the inhibition encountered during exposure of infected BSC cells to halothane or isoflurane was also investigated. In cultures exposed to halothane or enflurane, recovery of infectious virus synthesis was rapid and complete. Recovery of virus synthesis was slower after isoflurane removal and did not reach the peak control titers of infected cultures not exposed to the anesthetic. Treatment with halothane resulted in the formation of a preponderance of slowly sedimenting virus nucleocapsid particles which contained less than full-length ribonucleic acids after anesthetic removal. Neither enflurane nor isoflurane treatment of BSC cultures resulted in the formation of significant levels of these slowly sedimenting particles with short genomes after anesthetic removal.
在常用挥发性麻醉剂恩氟烷(2-氯-1,1,2-三氟乙基二氟甲醚)及其异构体异氟烷(1-氯-2,2,2-三氟乙基二氟甲醚)存在的情况下,研究了麻疹病毒在BSC细胞中的复制情况。在麻醉剂的临床浓度(高达4%)下,细胞分裂受到抑制,而仅观察到极小的细胞毒性作用。暴露于这些麻醉剂的细胞培养物中产生的子代病毒数量呈剂量相关减少。随着麻醉剂浓度增加,[³H]尿苷掺入麻疹病毒核衣壳的量也逐渐减少。在比较氟烷(2-溴-2-氯-1,1,1-三氟乙烷)、恩氟烷或异氟烷存在时对麻疹病毒复制的抑制作用时发现,感染后48小时传染性病毒出现的抑制以及[³H]尿苷掺入麻疹病毒核衣壳的情况均与麻醉剂浓度成正比。三种麻醉剂的等效麻醉浓度(最低肺泡浓度)产生同等程度的作用,但绝对浓度则不然。此外,还研究了感染的BSC细胞暴露于氟烷或异氟烷期间所遇抑制后传染性病毒合成的恢复情况。在暴露于氟烷或恩氟烷的培养物中,传染性病毒合成的恢复迅速且完全。去除异氟烷后病毒合成的恢复较慢,且未达到未暴露于麻醉剂的感染培养物的对照峰值滴度。用氟烷处理导致形成大量沉降缓慢的病毒核衣壳颗粒,去除麻醉剂后这些颗粒所含的核糖核酸长度小于全长。去除麻醉剂后,恩氟烷或异氟烷处理的BSC培养物均未导致形成大量具有短基因组的沉降缓慢的颗粒。