Background: Despite progress in the invasive treatment of ischemic heart disease, the ability to limit ischemia-reperfusion (I/R) injury remains largely unrealized. Ischemic pre-conditioning (IPC) and post-conditioning (POC) induce the protective mechanisms of resistance against I/R injury. Stimulation of opioid receptors mimic the protective effect of IPC or POC in an animal models. We tested the hypothesis, that IPC and POC provide cardioprotection in opioid-dependent mechanism in human myocardium.
Methods: Human atrial trabeculae were subjected to I/R injury. To achieve IPC, single hypoxia period preceded the applied lethal hypoxia, to achieve POC triple hypoxia periods followed lethal hypoxia. Naloxone was used at the onset of lethal hypoxia in IPC protocol, and at the time of re-oxygenation in POC protocol. Contractive function of the myocardium was assessed as maximal force of contraction (Amax), rate of rise of force of contraction (+dV/dT) and diastolic parameter - rate of decay of force of contraction (-dV/dT).
Results: Co-application of naloxone with IPC or POC resulted in decrease of Amax, +dV/dT and -dV/dT during re-oxygenation period as compared to IPC or POC only.
Conclusions: Naloxone abrogates beneficial effect of IPC and POC. IPC and POC in humans provide cardioprotection in opioid receptor system dependent mechanism.
Keywords: ischemia; naloxone; post-conditioning; pre-conditioning; reperfusion.