Why the study?
Does δ2-OR agonist deltorphin II increase cardiac resistance to reperfusion in non-adapted rats?
Does δ2-OR agonist deltorphin II increase cardiac resistance to reperfusion in non-adapted rats?
Activation of the δ2-opioid receptor with deltorphin II provides cardioprotection against reperfusion injury through specific protein kinase pathways in preclinical models.
δ2-OR activation may enhance reperfusion tolerance in models; leaves open clinical translation and human trials.
An analysis of published data and the results of our own studies showed that activation of peripheral δ2-opioid receptor (δ2-OR) increases cardiac tolerance to reperfusion. It has been established that this δ2-OR is localized in cardiomyocytes. Endogenous opioids are not involved in the regulation of cardiac resistance to reperfusion in non-adapted rats. The infarct-limiting effect of δ2-OR agonist deltorphin II depends on the activation of following protein kinases: PKCδ, ERK1/2, PI3K, PCG. SarcKATP channel and MPT pore are hypothetical end effectors of the cardioprotective effect of deltorphin II.
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Mukhomedzyanov et al. (2023) studied this question.
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