Heat stroke is characterized by
hyperthermia, arterial
hypotension, decreased baroreflex sensitivity, and increased serum levels of
beta-endorphin. Whereas
naltrexone may have therapeutic potential in
heat stroke, the underlying mechanism remains unclear. We tested the hypothesis that
naltrexone may attenuate
heat stroke by reducing
hyperthermia,
hypotension, decreased baroreceptor sensitivity, and/or increased serum levels of
beta-endorphin.
Heat stroke was induced by exposing the anesthetized adult Sprague-Dawley rats in an incubator at 43 degrees C. The moment in which the mean arterial pressure dropped irreversibly from the peak level was taken as the onset of
heat stroke. Control rats were exposed to 24 degrees C. Mean arterial pressure, baroreceptor sensitivity, and maximal reflex
bradycardia, after the onset of
heat stroke, were all significantly lower than in control rats. However, rectal temperature and serum levels of
beta-endorphin were all greater after the onset of
heat stroke. Intravenous delivery of
naltrexone (10 mg/kg) 20 min before the initiation of heat stress, but not immediately at the onset of
heat stroke, significantly attenuated the above-mentioned reactions. Accordingly,
naltrexone improved survival during
heat stroke. These results suggest that
naltrexone protects against
hypotension and decrement of both baroreceptor sensitivity and maximal reflex
bradycardia during
heat stroke by reducing both
hyperthermia and increment of serum
beta-endorphin and thus improves survival.