CA2-DEPENDENT OUTWARD CURRENTS IN MYOCYTES FROM EPICARDIAL BORDER ZONE OF 5-DAY INFARCTED CANINE HEART()

Myocytes from the epicardial border zone (EBZ) of the 5-day infarcted canine heart (IZ) have abnormal transmembrane action potentials, reduc ed L-type Ca2+ currents (I-Ca,I-L) and altered intracellular Ca2+ (Ca- i) transients compared with those of normal epicardial myocytes (NZ). We hypothesized that altered Ca-i cycling might be reflected in differ ences in Ca-i-dependent outward currents (I-to2). We recorded I-to2 in NZ and IZ using whole cell patch-clamp techniques. I-to2 was defined as the amplitude of the 4-aminopyridine-resistant transient outward cu rrent that was blocked by 200 mu M 4,4'-diisothiocyanostilbene-2,2'-di sulfonic acid (DIDS) or DIDS + ryanodine (2 mu M). I-toz were present in both NZ and IZ, but peak density was significantly reduced in IZ, p articularly at positive plateau voltages. Time course of decay of I-to 2 was biexponential and similar in NZ and IZ. A given peak I-ca,I-L wa s usually associated with a smaller peak I-to2 in IZ. These difference s were exaggerated when I-to2 and Ca-i transients were determined in r apidly paced cells. In summary, myocytes surviving in the EBZ of the i nfarcted heart have I-to2, yet they are reduced in density and can var y, particularly at fast pacing rates.