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.


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.
DiCarlo
A L
AL
Vitreous State Laboratories, Catholic University of America, Washington, DC 20064, USA.
Farrell
J M
JM
Litovitz
T A
TA
D000818:Animals; D002642:Chick Embryo; D004574:Electromagnetic Fields; D006360:Heat-Shock Proteins / Q000378:metabolism*; D006358:Hot Temperature; D000860:Hypoxia / Q000378:metabolism / Q000628:therapy; D017202:Myocardial Ischemia / Q000378:metabolism / Q000628:therapy*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000628:therapy*; D009206:Myocardium / Q000378:metabolism