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Fluorocarbons and cardiac arrhythmia: does difluorodichloromethane (FC 12) inhibit cardiac metabolism?
Abstract:
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.
Insights
Difluorodichloromethane (FC 12) does not affect cellular energy in rat hearts. This study investigated FC 12
Area of Science:
- Cardiovascular toxicology
- Biochemistry
- Cellular physiology
Background:
- Certain fluorocarbons, including difluorodichloromethane (FC 12), are known to negatively impact the cardiovascular system by reducing transmembrane ionic conductances in cardiac tissues.
- The potential effects of FC 12 on active transport, enzymatic activity, and cellular energy levels remain largely unexplored.
Purpose of the Study:
- To investigate whether difluorodichloromethane (FC 12) inhibits active transport and affects cellular energy metabolism in cardiac tissues.
- To determine the impact of FC 12 exposure on key energy metabolites: phosphocreatine (PC), adenosine triphosphate (ATP), and cyclic adenosine monophosphate (AMPc).
Main Methods:
- Rat hearts were used to measure concentrations of phosphocreatine (PC), adenosine triphosphate (ATP), and cyclic adenosine monophosphate (AMPc).
- Rats were divided into four groups: two control groups (breathing oxygen/nitrogen mixture, and oxygen/nitrogen with epinephrine) and two experimental groups where nitrogen was replaced by FC 12.
- FC 12 concentration in arterial blood was maximized at 720 micrograms/ml.
Main Results:
- Exposure to FC 12 at a maximal concentration of 720 micrograms/ml in arterial blood did not result in significant differences in PC, ATP, or AMPc levels.
- The concentrations of these key energy metabolites in the FC 12 exposed groups were comparable to those in the control groups.
Conclusions:
- Difluorodichloromethane (FC 12) does not appear to inhibit active transport or deplete cellular energy stores (PC, ATP, AMPc) in rat hearts at the tested concentrations.
- These findings suggest that the cardiovascular depressant effects of FC 12 are likely mediated through mechanisms other than the inhibition of cellular energy metabolism.