Fluorocarbons and cardiac arrhythmia: does difluorodichloromethane (FC 12) inhibit cardiac metabolism?
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.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced*; D002463:Cell Membrane Permeability / Q000187:drug effects; D005617:Chlorofluorocarbons, Methane / Q000633:toxicity*; D000242:Cyclic AMP / Q000096:biosynthesis; D006321:Heart / Q000187:drug effects*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D005617:Chlorofluorocarbons, Methane; D000242:Cyclic AMP; C007782:dichlorodifluoromethane