We investigated the effects of the opiate antagonist naloxone on the r
elease of beta-endorphin and cortisol in rats subjected to sepsis. Sep
sis was induced in weanling male Wistar albino rats (3-4 weeks old, 75
-90 g) by cecal ligation and double perforation (CLP). Forty animals w
ere randomly allocated to four groups. Group 1 was given naloxone hydr
ochloride 0.5 mg/kg subcutaneously after CLP and this treatment was re
peated at 2-h intervals until the rats were killed. Group 2 rats under
went a sham operation. Group 3 (control group) rats had CLP. Group 4 c
onsisted of nonoperated animals used to establish normal reference val
ues. Eighteen hours after CLP or sham operation, the rats were killed
by cervical dislocation and a blood sample was drawn via cardiac punct
ure to determine the beta-endorphin and cortisol levels. The beta-endo
rphin levels were significantly higher in the control group than in th
e sham-operated, naloxone-treated (NT), and nonoperated rats (P<0.05).
However, there were no significant differences in plasma beta-endorph
in levels between sham-operated, NT and nonoperated rats (P>0.05). Pla
sma cortisol levels were significantly higher in the control group com
pared with the other three groups and this difference was more signifi
cant in sham-operated and nonoperated rats (P<0.01). However, no diffe
rence Existed between sham-operated, NT, and nonoperated rats (P>0.05)
. This study demonstrates that the endogenous opioid system may play a
role in the activation of the pituitary-adrenal axis following sepsis
, and shows that the increase in beta-endorphin and cortisol could be
blocked by naloxone.