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A possible role for endogenous prostaglandins in the toxic electrophysiological effects of the aglycone acetylstrophanthidin was studied in isolated canine Purkinje fiber papillary muscle preparations by standard microelectrode techniques. Acetylstrophanthidin (5 X 10(-8) g/ml) caused a significant increase in 6-keto-prostaglandin F1 alpha release from these preparations. A significant loss of membrane potential and the development of oscillatory afterpotentials was observed, as well. Administration of either of two nonsteroidal antiinflammatory agents, indomethacin (3 X 10(-5) g/ml) or aspirin (5 X 10(-5) g/ml), in the presence of acetylstrophanthidin, abolished the stimulation of 6-keto-prostaglandin F1 alpha release and delayed and attenuated the loss of membrane potential and the development of oscillatory afterpotentials. In addition, indomethacin and aspirin appeared to preserve the electrogenic pumping capacity of Purkinje fiber cells exposed to acetylstrophanthidin. Exposure of Purkinje tissues to acetylstrophanthidin inhibited post-pacing hyperpolarization normally exhibited by these tissues. Both indomethacin and aspirin decreased this inhibition. Addition of prostacyclin (1 ng/ml) after 30 minutes of exposure to acetylstrophanthidin to preparations in which endogenous prostaglandin synthesis had been inhibited, resulted in a significant increase in the amplitude of oscillatory afterpotentials within 2 minutes. These results suggest that the presence of endogenous prostaglandins may play a role in the development of the toxic electrophysiological effects associated with acetylstrophanthidin.

A possible role for endogenous prostaglandins in the electrophysiological effects of acetylstrophanthidin on isolated canine ventricular tissues.