Lessard Y, Begue J M, Paulet G
Acta Pharmacol Toxicol (Copenh). 1986 Jan;58(1):71-3. doi: 10.1111/j.1600-0773.1986.tb00072.x.
Certain fluorocarbons, such as difluorodichloromethane (FC 12), depress the cardiovascular system by diminution of all the transmembrane ionic conductances in cardiac tissues. Does FC 12 also inhibit active transport and thus enzymatic activity and cellular energy? We measured phosphocreatine (PC), adenosine triphosphate (ATP) and cyclic adenosine monophosphate (AMPc) in rat hearts. Rats were randomly divided into 4 groups; 2 control groups: one breathing a mixture of oxygen (21%) and nitrogen (79%) (group C) and the other breathing the same mixture but simultaneously perfused with 1 microgram/kg/min. epinephrine (groupe E-C); 2 trial groups T and E-T where nitrogen was replaced by FC 12. The maximal FC 12 concentration of 720 micrograms/ml in arterial blood produced no significant difference in the concentrations of these three metabolites compared with controls.
某些碳氟化合物，如二氟二氯甲烷（FC 12），通过降低心脏组织中所有跨膜离子电导来抑制心血管系统。FC 12是否也抑制主动转运，从而抑制酶活性和细胞能量？我们测量了大鼠心脏中的磷酸肌酸（PC）、三磷酸腺苷（ATP）和环磷酸腺苷（AMPc）。大鼠被随机分为4组；2个对照组：一组呼吸氧气（21%）和氮气（79%）的混合物（C组），另一组呼吸相同混合物但同时灌注1微克/千克/分钟的肾上腺素（E-C组）；2个试验组T和E-T，其中氮气被FC 12取代。与对照组相比，动脉血中FC 12的最大浓度720微克/毫升在这三种代谢物的浓度上没有产生显著差异。
