Key result
Naloxone treatment in the acute stage of experimental autoimmune myocarditis decreased cardiac pathology and inflammatory cytokines compared to untreated mice, but showed no benefit in the chronic stage.
Why the study?
Does naloxone improve cardiac pathology and reduce inflammation in mice with experimental autoimmune myocarditis?
Does naloxone improve cardiac pathology and reduce inflammation in mice with experimental autoimmune myocarditis?
Naloxone demonstrates beneficial effects in the acute stage of experimental autoimmune myocarditis in mice by reducing lymphocyte cytotoxic activities and modulating neurohumoral responses.
Hypothesis-generating for acute immunomodulation in myocarditis models; leaves open chronic efficacy and human translation.
Little is known about effects of naloxone, an opiate receptor antagonist, upon experimental autoimmune myocarditis (EAM) in mice. The aim of the present study was to test the effects of naloxone upon EAM in mice. Four-week-old C57BL/6 mice were injected with porcine cardiac myosin. Naloxone 1 mg/kg/day was given intraperitoneally daily on days 0 to 21 in experiment I (acute stage) and on days 21 to 42 in experiment II (chronic stage). For the analysis of endogenous opiate and neurohumoral system, plasma beta-endorphin and cytokines were measured. The cytotoxic activity of lymphocytes was determined by Cr-release assay. Naloxone reversed hypotension produced by massive myocardial injury in experiment I. In experiment I, the severity of cardiac pathology and inflammatory cytokines were decreased in the naloxone-treated group associated with higher beta-endorphin level compared with the untreated group. In addition, naloxone induced a shift from Th1 cytokine toward Th2 cytokine balance. Thus, cytotoxic activities of lymphocytes against EL-4 tumor cells were lower in the treated group than in the untreated group in experiment I, but not in experiment II. Naloxone is beneficial for heart failure caused by EAM in the acute stage, but not in the chronic stage, due to decreasing cytotoxic activities of lymphocytes and to its neurohumoral modulating effects.
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Kishimoto et al. (2008) studied Experimental autoimmune myocarditis (EAM). Naloxone vs. Untreated group was evaluated on Severity of cardiac pathology, inflammatory cytokines, and cytotoxic activity of lymphocytes. Naloxone treatment in the acute stage of experimental autoimmune myocarditis decreased cardiac pathology and inflammatory cytokines compared to untreated mice, but showed no benefit in the chronic stage.
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