Effect of chronic left ventricular failure on β-endorphin

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.