The objectives of this study were to investigate the role of
endogenous opioids in the mediation of stress-induced
cardiomyopathy (SIC), and to evaluate which opioid receptors
regulate heart resistance to immobilization stress. Wistar rats
were subjected to 24 h immobilization stress. Stress-induced
heart injury was assessed by 99mTc-pyrophosphate accumulation
in the heart. The opioid receptor (OR) antagonists (naltrexone,
NxMB – naltrexone methyl bromide, MR 2266, ICI 174.864) and
agonists (DALDA, DAMGO, DSLET, U-50,488) were administered
intraperitoneally prior to immobilization and 12 h after the start
of stress. In addition, the selective µ OR agonists PL017 and
DAMGO were administered intracerebroventricularly prior to
stress. Finally pretreatment with guanethidine was used.
Naltrexone did not alter the cardiac 99mTc-PP accumulation in
stressed rats. NxMB aggravated stress-induced cardiomyopathy
(P=0.005) (SIC). The selective µ OR agonist DALDA, which does
not cross the blood-brain barrier, completely prevented
(P=0.006) SIC. The µ OR agonist DAMGO exhibited weaker effect
than DALDA. The selective δ ligand (DSLET) and κ OR ligand
(U-50,488) did not alter stress-induced 99mTc-pyrophosphate
accumulation in the heart. Intracerebroventricular administration
of the µ OR agonists aggravated SIC. Pretreatment with
guanethidine abolished this effect (P=0.01). Guanethidine alone
exhibited cardioprotective properties. A stimulation of central
µ OR promotes an appearance of SIC. In contrast, stimulation of peripheral µ OR contributes to an increase in cardiac tolerance to
stress