beta-endorphin and Heat-Stroke

It has been suggested that a proopiomelanocortin peptide beta-endorphin may play an important role in temperature regulation and therefore have specific heat stroke response patterns.. The purpose of this study was to examine the response patterns of plasma beta-endorphin at baseline, during a 7-d exercise-heat acclimation period (HA; 90 min x d(-1), 40 degrees C), and during a 6-h exercise-heat tolerance test (HTT; 6 h, 40 degrees C) performed before and after HA. Subjects were nine previously diagnosed heatstroke patients (P) and eight matched controls (C). No differences between the two groups were observed at rest, prior to HTT.. Plasma beta-endorphin concentration in P significantly increased above resting values at 2, 4, and 6 h of HTT and were significantly greater than C responses. During HA tests, a significantly higher beta-endorphin concentration was observed in P before exercise on day 1 and day 7, but not on day 4. A significant increase occurred after exercise in both groups, on all days of HA; no differences were observed between the groups on days 4 and 7.. These results demonstrate that the opioid peptide responses in individuals with recent exertional heatstroke were greater than control subjects during the initial 6-h HTT. Decreased physical training among P may have contributed to these results. However, 7 d of HA abolished these between-group differences by reducing the magnitude of beta-endorphin responses in P, indicative of an adaptation of pituitary function.

Topics: Acclimatization; Adult; beta-Endorphin; Body Temperature Regulation; Exercise; Heat Stroke; Humans; Reference Values

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.

Topics: Animals; beta-Endorphin; Blood Pressure; Fever; Heart Rate; Heat Stroke; Hypotension; Male; Naltrexone; Narcotic Antagonists; Pressoreceptors; Rats; Rats, Sprague-Dawley