Effects of naloxone on beta-endorphin and cortisol release in sepsis

OKUR H., Küçükaydın M., Bozkurt A., Muhtaroğlu S.

RESEARCH IN EXPERIMENTAL MEDICINE, vol.196, no.4, pp.247-250, 1996 (Peer-Reviewed Journal) identifier

  • Publication Type: Article / Article
  • Volume: 196 Issue: 4
  • Publication Date: 1996
  • Journal Indexes: Science Citation Index Expanded
  • Page Numbers: pp.247-250


We investigated the effects of the opiate antagonist naloxone on the release of beta-endorphin and cortisol in rats subjected to sepsis. Sepsis was induced in weanling male Wistar albino rats (3-4 weeks old, 75-90 g) by cecal ligation and double perforation (CLP). Forty animals were randomly allocated to four groups. Group 1 was given naloxone hydrochloride 0.5 mg/kg subcutaneously after CLP and this treatment was repeated at 2-h intervals until the rats were killed. Group 2 rats underwent a sham operation. Group 3 (control group) rats had CLP. Group 4 consisted of nonoperated animals used to establish normal reference values. Eighteen hours after CLP or sham operation, the rats were killed by cervical dislocation and a blood sample was drawn via cardiac puncture to determine the beta-endorphin and cortisol levels. The beta-endorphin levels were significantly higher in the control group than in the sham-operated, naloxone-treated (NT), and nonoperated rats (P<0.05). However, there were no significant differences in plasma beta-endorphin levels between sham-operated, NT and nonoperated rats (P>0.05). Plasma cortisol levels were significantly higher in the control group compared with the other three groups and this difference was more significant in sham-operated and nonoperated rats (P<0.01). However, no difference 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.