In rat myocytes 3 weeks post-myocardial infarction, depressed Na+/Ca2+ exchange activity significantly prolonged the half-time of relaxation compared to sham (1.54 vs 1.10 s, P<0.02).
Depressed Na+/Ca2+ exchange activity contributes to abnormal cellular contractile behavior and prolonged relaxation in post-myocardial infarction rat myocytes.
Absolute Event Rate: 1.54% vs 1.1%
p-value: p=<0.02
The significance of altered Ca2+ influx and efflux pathways on contractile abnormalities of myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) was investigated by varying extracellular Ca2+ concentration (Ca2+o, 0.6-5.0 mM) and pacing frequency (0.1-5.0 Hz). Myocytes isolated from 3-wk MI hearts were significantly longer than those from sham-treated (Sham) hearts (125 +/- 1 vs. 114 +/- 1 micrometer, P < 0.0001). At high Ca2+o and low pacing frequency, conditions that preferentially favored Ca2+ influx over efflux, Sham myocytes shortened to a greater extent than 3-wk MI myocytes. Conversely, under conditions that favored Ca2+ efflux (low Ca2+o and high pacing frequency), MI myocytes shortened more than Sham myocytes. At intermediate Ca2+o and pacing frequencies, differences in steady-state contraction amplitudes between Sham and MI myocytes were no longer significant. Collectively, the interpretation of these data was that Ca2+ influx and efflux pathways were subnormal in MI myocytes and that they contributed to abnormal cellular contractile behavior. Because Na+/Ca2+ exchange activity, but not whole cell Ca2+ current, was depressed in 3-wk MI rat myocytes, our results on steady-state contraction are consistent with, but not proof of, the hypothesis that depressed Na+/Ca2+ exchange accounted for abnormal contractility in MI myocytes. The effects of depressed Na+/Ca2+ exchange on MI myocyte mechanical activity were further evaluated in relaxation from caffeine-induced contractures. Because Ca2+ uptake by sarcoplasmic reticulum was inhibited by caffeine and with the assumption that intracellular Na+ and membrane potential were similar between Sham and MI myocytes, myocyte relaxation from caffeine-induced contracture can be taken as an estimate of Ca2+ extrusion by Na+/Ca2+ exchange. In MI myocytes, in which Na+/Ca2+ exchange activity was depressed, the half time of relaxation (1.54 +/- 0.14 s) was significantly (P < 0.02) prolonged compared with that measured in Sham myocytes (1.10 +/- 0.10 s).
Zhang et al. (Mon,) conducted a other in Myocardial infarction. Myocardial infarction vs. Sham treatment was evaluated on Half time of relaxation from caffeine-induced contractures (p=<0.02). In rat myocytes 3 weeks post-myocardial infarction, depressed Na+/Ca2+ exchange activity significantly prolonged the half-time of relaxation compared to sham (1.54 vs 1.10 s, P<0.02).