Abstract
ICa in Healed Myocardial Infarction. Introduction: Abnormal action potentials in myocytes adjacent to > 2‐month‐uld feline LV myocardial infarcts (MI) may reflect alterations in Ca2+ currents (ICa).
Methods and Results: We compared ICa, at 36°C, in subendocardial myocytes isolated from areas adjacent to MI and to ICa in cells from remote areas (> 4 mm away; REM) and control cells from similar regions in normal hearts. Control (CON) myocytes had membrane capacitance of 234 ± 10 pF (n = 81 cells) compared to 305 ± 14 pF in REM (71 cells; P < 0.05 from CON) and 237 ± 11 pF (n = 55 cells) in MI (not different from CON). From Vh=−40 mV, peak ICa elicited by test potentials (−35 to +70 mV) were significantly larger in CON (−1746 ± 123 pA) and REM (−1795 ± 142 pA) compared to Ml (−1352 ± 129 pA) (P < 0.05). Peak 1(11 density was significantly reduced in REM (−6.0 ± 0.4 pA/pF) or MI (−5.7 ± 0.4 pA/pF, P < 0.05) compared to CON (−7.5 ± 0.4 pA/pF). Double exponential ICa decay was similar among groups. Half‐inactivation potential (V0.5) was significantly shifted (hyperpolarizing direction) for MI (−29.1 ± 2.6 mV) and REM (−24.6 ± 1.2 mV) myocytes compared to −20.3 ± 1.0 mV in CON. MI slope factor (k; 9.0 ± 0.5) was significantly different from CON (6.8 ± 0.3) and RKM (7.3 ± 0.4). No differences in time course of recovery from inactivation were noted. Five millimolar Ba2+0 produced significant increases in ICa in CON and REM but an attenuated response in MI. Bay k8644 (1 μM) produced similar ICa increase in all groups. ICa increase due to isoproterenol (1 ICaM) in MI and REM was half that in CON, but there were no differences in increased ICa responses among groups following phenylephrine (10 μM).
Conclusion: Reduced ICa density in REM reflects cell hypertrophy, whereas altered ICa of MI may reflect altered channel structure and/or function.
