Brabec M J, Bedows E, Davidson B A, Knight P R
Anesthesiology. 1984 Jul;61(1):43-7.
The authors examined the inhibition of aerobic metabolism in monkey kidney cell cultures exposed to halothane, enflurane, and isoflurane. The ability of hyperbaric pressure to reverse the halothane-induced metabolic inhibition also was examined. Incubation of two monkey kidney cell lines for 24 h with clinically equipotent concentrations (2.6 MAC) of halothane, enflurane, or isoflurane vapors increased the concentration of lactate in the media by 126 to 244% relative to nonexposed control cultures. The increased rate of lactate accumulation was proportional to the concentration of halothane and was accompanied by a decrease in media pH. Removal of halothane restored the normal rate of lactate production. Hyperbaric pressures of 25, 50, and 100 atmospheres did not alter the halothane-stimulated rate of lactate production relative to non-anesthetic-treated controls, although pressure alone did depress the rate of lactate accumulation in all cultures. The stimulation of lactate production likely reflects the known ability of halothane to inhibit mitochondrial respiration. The failure of pressure to reverse the stimulation of lactate production by halothane suggests that inhibition of mitochondrial metabolism cannot be reversed by pressure.
作者研究了氟烷、恩氟烷和异氟烷对猴肾细胞培养物中需氧代谢的抑制作用。还研究了高压逆转氟烷诱导的代谢抑制的能力。用临床等效浓度（2.6MAC）的氟烷、恩氟烷或异氟烷蒸汽孵育两种猴肾细胞系24小时，相对于未暴露的对照培养物，培养基中乳酸浓度增加了126%至244%。乳酸积累速率的增加与氟烷浓度成正比，并伴有培养基pH值的降低。去除氟烷后，乳酸产生恢复正常速率。相对于未用麻醉剂处理的对照，25、50和100个大气压的高压并未改变氟烷刺激的乳酸产生速率，尽管单独的压力确实会降低所有培养物中乳酸的积累速率。乳酸产生的刺激可能反映了氟烷抑制线粒体呼吸的已知能力。压力未能逆转氟烷对乳酸产生的刺激作用，这表明压力无法逆转线粒体代谢的抑制作用。
