Abstract
Background Reperfusion of the myocardium is imperative to limit the damage caused, by occlusion of an artery following myocardial infarction (MI). However, restoration of blood flow to the ischaemic tissue causes damage itself, a phenomenon known as reperfusion injury. Modifying cellular processes at early reperfusion can reduce the irreversible cell damage caused. The reperfusion injury salvage kinase (RISK) pathway, an endogenous signalling pathway that is activated during early reperfusion to limit lethal damage is a pharmacological target. Soluble guanylyl cyclase (sGC) – cyclic guanosine monophosphate (cGMP) is a component of the RISK pathway. Previous studies have shown that the cGMP analogue 8Br-cGMP limits infarct size when given at reperfusion in an experimental model of MI [1]. We therefore hypothesised that administration of the sGC stimulator BAY 412272 or the sGC activator BAY 602770 at reperfusion would be cardioprotective, limiting infarct size.
Highlights
Reperfusion of the myocardium is imperative to limit the damage caused, by occlusion of an artery following myocardial infarction (MI)
Following reperfusion hearts were frozen, sliced into disks and stained with triphenyltetrazolium chloride and infarct size was expressed as a percentage of the ischaemic risk zone
To confirm that BAY 412272 elevated cyclic guanosine monophosphate (cGMP), radioimmunoassay was carried out on myocardial tissue samples perfused with BAY 412272 at early reperfusion
Summary
Reperfusion of the myocardium is imperative to limit the damage caused, by occlusion of an artery following myocardial infarction (MI). ODQ was perfused with or without BAY 412272 and ODQ with or without BAY 602770. Following reperfusion hearts were frozen, sliced into disks and stained with triphenyltetrazolium chloride and infarct size was expressed as a percentage of the ischaemic risk zone.
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