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.