Effects of broad band electromagnetic fields on HSP70 expression and ischemic-reperfusion in rat hearts

Although exposure to broad band (0.2-20 MHz) electromagnetic fields (EMF) is part of the treatment of several diseases, little is known as to their effects on myocardial protein expression and resistance to ischemia-reperfusion (I/R). We exposed Sprague-Dawley rats to either high (H, 10 min/day at 200 V/m, 36.1 μT) or low (L, 2 min/day at 30 V/m, 11.4 μT) intensity broad band EMF for 15 days. At the end of the treatment, myocardial HSP70 was 32 ± 8% (mean ± SEM) higher in L (P = 0.01) than in control (C), whereas in H it remained the same as in C. Electron microscopy revealed sporadic ruptures of mitochondrial cristae in H hearts, with no differences in other parameters. Malondialdehyde was increased in treated hearts (P < 0.05), but especially in H (P = 0.008). To assess the protective role of HSP70 during I/R, hearts were Langendorff-perfused with Krebs-Henseleit. After I/R, C hearts displayed depressed rate·pressure (-13 ± 7%) and increased end-diastolic (+9.2 ± 2.8 mmHg) and perfusion pressures (+30 ± 10 mmHg). In H and L, rate·pressure recovery was similar to C (-2 ± 21% and -12 ± 16%, respectively, P = NS). In contrast, both end-diastolic and perfusion pressures were higher in L than in H (30.8 ± 5.4 vs 18.2 ± 3.5, P = 0.01, and 54 ± 8 vs 21 ± 8 mmHg, P = 0.01, respectively) indicating diastolic derangement in L. In conclusion, the effects of broad band EMF on HSP70 appear to be biphasic, and HSP70 overexpression might not be directly related to improved protection against I/R.