Beta endorphin, a vasoconstrictor during septic shock

Sue Doty, Lillian Traber, David Herndon, Ryozo Kimura, Hans Lubbesmeyer, Susan Davenport, Daniel L. Traber

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

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. Chronically instrumented sheep were given E. coli endotoxin (LPS, 1.5 mcg/kg × 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. 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 posttreatment with naloxone lessened the maximum increase in total peripheral resistance index compared with untreated sheep. 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 - Injury, Infection and Critical Care
Volume28
Issue number2
DOIs
StatePublished - Feb 1988

ASJC Scopus subject areas

  • Surgery
  • Critical Care and Intensive Care Medicine

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    Doty, S., Traber, L., Herndon, D., Kimura, R., Lubbesmeyer, H., Davenport, S., & Traber, D. L. (1988). Beta endorphin, a vasoconstrictor during septic shock. Journal of Trauma - Injury, Infection and Critical Care, 28(2), 131-139. https://doi.org/10.1097/00005373-198802000-00001