Effect of chronic left ventricular failure on β-endorphin

E. Mellow, E. Redei, K. Marzo, J. R. Wilson*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

Stimulation of endogenous opiate secretion worsens circulatory dysfunction in several forms of shock, in part by inhibiting sympathetic activity. To investigate whether endogenous opiates have a similar effect in chronic heart failure (HF), we measured β-endorphin concentrations and hemodynamic responses to naloxone infusion (2 mg/kg bolus + 2 mg · kg-1 · h-1) in six control (C) dogs and eight dogs with low-output HF produced by 3 wk of rapid ventricular pacing. The dogs with HF exhibited reduced arterial blood pressure (C, 123 ± 4 vs. HF, 85 ± 7 mmHg; P < 0.01) and cardiac outputs (C, 179 ± 14 vs. HF, 76 ± 2 ml · min-1 · kg-1; P < 0.01) and elevated plasma norepinephrine concentrations (C, 99 ± 12 vs. HF, 996 ± 178 pg/ml; P < 0.01) but normal β-endorphin concentrations (C, 30 ± 11 vs. HF, 34 ± 12 pg/ml; P = NS). Naloxone produced similar transitory increases in blood pressure (C, 14 ± 5 vs. HF, 26 ± 25%) and cardiac output (C, 37 ± 13 vs. HF, 22 ± 15%) in both groups (both P = NS). No significant changes in norepinephrine concentration or systemic vascular resistance were observed in either group. These findings suggest that β-endorphin secretion does not exacerbate circulatory dysfunction in chronic heart failure.

Original languageEnglish (US)
Pages (from-to)2675-2680
Number of pages6
JournalJournal of applied physiology
Volume73
Issue number6
StatePublished - 1992

Keywords

  • naloxone
  • sympathetic activity

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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