Arrhythmogenic and antiarrhythmic effects of lipolytic factors on cultured heart cells.

Lipolytic factors associated with myocardial ischemia and factors which activate phospholipase A2 in cells other than heart cells were tested for their actions on the rhythmicity of cultured heart cells. Exogenous triglyceride lipase was without a significant effect on beating while phospholipase A2 produced concentration-related arrhythmias in concentrations as low as 0.0375 U/ml. Quinacrine, a phospholipase inhibitor, demonstrated concentration-dependent inhibition of reoxygenation-induced arrhythmias. Of the compounds known to activate phospholipase only kallikrein and thrombin produced arrhythmias; only bradykinin, thrombin and trypsin depressed beating. Lysophosphatidylcholine, a reaction product of phospholipase A2 on phospholipids, inhibited reoxygenation arrhythmias in a concentration-dependent manner.