Beta endorphin, a vasoconstrictor during septic shock

S. Doty, L. Traber, David Herndon, R. Kimura, H. Lubbesmeyer, S. Davenport, D. Traber

Research output: Contribution to journalArticle

10 Scopus citations


A relationship between increased peripheral resistance (TPRI) and decreased cardiac index (CI) and mortality from sepsis has been suggested. The relationship between endogenous opiates and this response was evaluated. Methods: Chronically instrumented sheep were given E. coli endotoxin (LPS, 1.5 mcg/kg x 30 minutes). In one study, survivors (n = 9) and nonsurvivors (n = 11) of LPS were compared along with survivors (n = 8) of half the dose of LPS. In a second study, two groups of animals received naloxone: one (n = 11) had a bolus of 2 mg/kg followed by a 2 mg/kg/hr continuous infusion started 30 minutes before LPS while the other had the bolus and infusion started 1 hour after LPS was begun. Results: Both vasoconstrictive and vasodilative phases were seen. Vasoconstriction was associated with elevated beta endorphin levels, a pattern sustained until death in the nonsurvivors. Both pre- and post-treatment with naloxone lessened the maximum increase in total peripheral resistance index compared with untreated sheep. Discussion: The vasoconstrictive aspects of the response to LPS correlated with elevated beta endorphin levels and with mortality. This vascular response is attenuated with naloxone blockade.

Original languageEnglish (US)
Pages (from-to)131-139
Number of pages9
JournalJournal of Trauma
Issue number2
StatePublished - 1988


ASJC Scopus subject areas

  • Surgery

Cite this

Doty, S., Traber, L., Herndon, D., Kimura, R., Lubbesmeyer, H., Davenport, S., & Traber, D. (1988). Beta endorphin, a vasoconstrictor during septic shock. Journal of Trauma, 28(2), 131-139.