A proposed mechanism for cardiac sensitisation: electrophysiological study of effects of difluorodichloromethane and adrenaline on different types of cardiac preparations isolated from sheep hearts.

Difluorodichloromethane (FC12) inhaled at high concentrations sensitises, as do numerous other volatile organic compounds, mammalian heart to adrenaline induced arrhythmias. In this study three types of cardiac tissue (spontaneously beating sinusal and Purkinje preparations and stimulated Purkinje fibres) were isolated from sheep hearts and perfused for electrophysiological recording to examine the effect of FC 12. Preparations were perfused alternately with a control solution of physiological fluid and a trial solution with dissolved FC 12, the partial pressure of oxygen remaining identical.

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.

Mechanism of liposoluble drugs and general anaesthetic's membrane action: action of difluorodichloromethane (FC 12) on different types of cardiac fibres isolated from sheep hearts.

The effect of difluorodichloromethane (FC 12), a chemically stable aerosol propellant which has long been considered innocuous, on several types of cardiac fibres isolated from sheep hearts after preparation in a nutritive solution was studied. Modifications in resistance and transmembrane potentials suggested a mechanism of FC 12 action. Physical constraint on membrane structures produced by high FC 12 concentrations from simple dissolution in the internal lipid layer explain modifications in cardiac membrane properties.