Why the study?
Does Bay Y5959 alter L-type Ca2+ currents and intracellular Ca2+ transients in surviving epicardial cells from infarcted canine hearts?
Does Bay Y5959 alter L-type Ca2+ currents and intracellular Ca2+ transients in surviving epicardial cells from infarcted canine hearts?
Bay Y5959 restores L-type Ca2+ currents in surviving cells of the infarcted epicardial border zone, potentially contributing to antiarrhythmic effects against reentrant ventricular tachycardias.
May suggest antiarrhythmic potential in canine infarct models; leaves open translation to human therapy.
We determined and compared the effects of the dihydropyridine agonist, Bay Y5959, on the amplitude of L-type Ca2+ currents and intracellular Ca2+ transients in epicardial cells from noninfarcted hearts (NZs) and surviving cells from the epicardial border zone of 5-day infarcted canine hearts (IZs). We determined the effects of Bay Y5959 on the L-type Ca2+ current by using single cells and a whole-cell voltage-clamp approach. To elucidate the effects of Bay Y5959 on the amplitude and time course of the spatially averaged intracellular Ca2+ transient (Ca(i)T), myocytes from the two cell groups were loaded and studied by using the Ca2+-sensitive indicator fura-2/AM. Bay Y5959 increased the amplitude of the L-type Ca2+ current in both cell groups, but peak amplitude in NZs was always greater than that in IZs. Bay Y5959 also increased Ca(i)T amplitude in both NZs and IZs and significantly accelerated the Ca(i)T time course in IZs, particularly at the faster pacing-cycle length. We suggest that the Bay Y5959 effect to restore L-type Ca2+ currents in IZs contributes to its observed antiarrhythmic effects during the reentrant ventricular tachycardias that are known to occur in the epicardial border zone of the infarcted heart.
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Pu et al. (1999) studied this question.
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