OXYGEN POISONING IN CARDIAC TISSUE

Abstract

Expts. are described in which contractions of isolated non-circulated frog hearts exposed to O2 at 70 and 80 lbs. gauge pressure were recorded. O2 at these pressures caused an initial increase and a slight but very late decrease, in the strength of ventricular contraction; a delayed (3-6 hrs.) slowing in frequency and an eventual complete cessation of automaticity. That the pace-setting mechanism was more susceptible to this "direct" deleterious effect of high O2 than was the contraction mechanism was shown by the persistence of cardiac muscle irritability to electrical stimulation long after the automatic beat had failed. The conductivity in excised hearts was initially improved by O2 at high barometric pressure. Possible late effects on the conductive mechanism were not apparent in these expts. Decompression to atmospheric pressure begun after the onset of the slowing but before complete cessation of the automatic beat, was frequently followed by either a definite recovery, or a stoppage of any further decrease in frequency. Decompression of itself begun after complete cessation of the automatic beat, invariably failed to bring about any evident recovery. Single shock stimuli applied to the heart after it had been stopped by a maintained pressure failed to induce any persistent recovery of the pace-setter though the muscle itself remained irritable. Similar stimulation applied following decompression, however, induced a more or less permanent recovery of automaticity. Recovery of the automaticity of submerged hearts previously stopped by high O2 pressure in Ringer soln., was induced without auxiliary stimulation by replacing the high O2 pressure soln. by a similar one equilibrated with O2 at atmospheric pressure. The "direct" toxic influence of high O2 pressure demonstrated in isolated hearts contributed to the cardiac effects observed in intact animals exposed for long periods, to O2 at high pressure, but it would seem to be of less significance in such cases than the disturbed carriage of CO2. This "direct" toxic effect was apparently cumulative and not completely reversible after prolonged exposures. Evidence was cited in support of the possibility that this "direct" toxic action involved a poisoning of respiratory enzymes.