Myocardial protection conferred by electromagnetic fields.
BACKGROUND: It has been reported that electromagnetic (EM) fields induce stress proteins in vitro. These proteins have been shown to be important in recovery from ischemia/reperfusion. It was, therefore, hypothesized that EM fields could activate stress responses in vivo and protect myocardial tissue during anoxia. METHODS AND RESULTS: Chick embryos were exposed to 4-, 6-, 8-, and 10- microT and 60-Hz EM fields for 20 minutes followed by a 1-hour rest period before placement in an anoxic chamber. Embryos were reoxygenated when survival of controls dropped to <40%, and final observations were made 30 minutes later. Data from 80 experiments (>500 EM field-exposed embryos) indicated that EM field protection was extremely significant (P<0.0001). Survival rates were 39.6% in controls and 68.7% in field-exposed embryos. In a second set of experiments, embryos were exposed for 20 minutes to several pretreatments: (1) hyperthermia (43 degreesC), (2) 60-Hz, 8- microT EM fields, or (3) 60-Hz, 8- microT EM fields plus a random EM noise field (8 microT). Embryo survival was 37.7% (control), 57.6% (heated), 69% (60-Hz EM field only), and 41.5% (60-Hz EM field plus EM noise). To confirm that heating resulting from field exposures did not occur, thermocouples were placed into several eggs at the site of the embryo during exposure; no increase in temperature was noted. CONCLUSIONS: We conclude that athermal EM field exposures induce stress responses that protect chick embryo myocardium from anoxia damage. These results suggest that EM field exposures may be a useful, noninvasive means of minimizing myocardial damage during surgery, transplantation, or heart attack in humans.