Ischemic heart disease and myocardial infarction continue to be leading causes of cardiovascular morbidity and mortality. Activation
of opioid, adenosine, bradykinin, adrenergic and other G-protein coupled receptors has been found to be cardioprotective. κ-
and/or δ-opioid receptor activation is involved in direct myocardial protection, while the role of µ-opioid receptors seems less clear. In
addition, differential affinities to the three opioid-receptor subtypes by various agonists and cross-talk among different G-protein coupled
receptors render conclusions regarding opioid-mediated cardioprotection challenging. The present review will focus on the protective effects
of endogenously released opioid peptides as well as exogenously administered opioids such as morphine, fentanyl, remifentanil, butorphanol,
and methadone against myocardial ischemia/reperfusion injury. Receptor heterodimerization and cross-talk as well as interactions
with other cardioprotective techniques will be discussed. Implications for opioid-induced cardioprotection in humans and for future
drug development to improve myocardial salvage will be provided.
Keywords: Butorphanol, cross-talk, enkephalin, fentanyl, heterodimerization, ischemia-reperfusion injury, opioid receptors, methadone,
morphine, myocardial, remifentanil.
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