Abstract

The effects of the negative inotropic agent, diacetyl monoxime (DAM), were studied on cardiac action potentials in young (3 day old) and old (13–18 day old) embryonic chick hearts and in rabbit papillary muscles. DAM (5–10 mM) decreased the action potential (AP) amplitude, the maximum rate of rise (Vmax), and AP duration of slow and fast APs in both young and old embryonic chick hearts. Concomitantly with these changes, the spontaneous beating rate was increased in young hearts. At 20 mM DAM, the maximum diastolic potential (MDP) was decreased. In fast APs of old embryonic chick hearts, the most prominent effect of DAM was a shortening of AP duration, the effects on AP amplitude, Vmax, and resting potential being less. In rabbit papillary muscles, DAM had little effect on the slow AP parameters except for shortening of AP duration. The onset of the DAM effects was rapid, the peak effect being attained within 10 min. We conclude that DAM suppressed the slow Na+ current present in young chick embryonic hearts. The effects of DAM, up to 10 mM, on Vmax of the fast Na+-dependent APs in old embryonic chick hearts was less, and there was no effect on rabbit hearts. DAM suppressed the slow Ca2+-dependent APs in old embryonic chick hearts but not in rabbit papillary muscles, suggesting that the effect of DAM on the Ca2+ slow channels depends on the species. The negative inotropic effects of DAM in chick hearts can be explained at least in part by inhibition of the Ca2+ influx through the slow channels.

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