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. Variable effects of FC 12 with localisation and time on automatism, excitability, and conduction in various types of cardiac tissue agreed with earlier observations of the depressive and arrhythmia effect of this gas on isolated and in situ 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. Sensitisation to adrenaline was studied by injecting adrenaline at a dose causing a notable effect without producing arrhythmias in the control preparations. Examination of transmembrane potential recordings confirmed that FC 12 inhibits sinus node pacemaker stimulation by adrenaline. Conversely, the adrenaline induced acceleration of latent pacemakers in certain types of Purkinje fibres appeared to be potentialised by FC 12. The various types of arrhythmia observed in vitro were explained by the effect of FC 12 on cell membranes, an affect which can oppose or favour that of adrenaline. These phenomena explain the arrhythmias observed in isolated hearts or whole animal preparations and permit a better understanding of the mechanism involved in cardiac sensitisation to adrenaline induced arrhythmia, a mechanism in which variability in time and location is the essential factor in the FC 12 effect.
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