ESPE Abstracts

Background: Timely reperfusion of ischaemic tissue is prerequisite to improve outcomes of CVD, but paradoxically reperfusion causes injury to tissues. This concept is referred to as ischaemia-reperfusion (IR) injury. Studies are thriving to better understand IR injury and develop novel treatments to minimise this. One such approach is termed ischaemic preconditioning (IPC) which entails brief periods of alternating ischaemia and reperfusion prior to the prolonged period of index ischaemia. Endogenous opioid peptides (EOPs) are thought to play a role in (IPC).

Aims: Using a human forearm model of IR injury this work assessed the effect of the non-selective opioid receptor antagonist, Naloxone, on protection by IPC. In addition, plasma concentrations of the endogenous opioid, Beta-Endorphin (β-EP), were assessed during an IPC stimulus.

Methods: The role of opioid receptor blockade, Naloxone in Ischaemic Preconditioning (IPC) on healthy volunteers was determined. Flow Mediated Dilatation (FMD) of the brachial artery was measured by ultrasound to determine endothelial IR injury. Using Enzyme-Linked Immunosorbent Assay (ELISA), β-EP was quantified to establish whether it has a local effect to induce protection during IR injury. Venous blood samples were collected from healthy volunteers during an IPC stimulus.

Results: IR caused endothelial dysfunction (FMD 6.7±0.7 pre- vs 2.5±0.4 post-IR, P <0.001, n = 10); IPC prevented IR-induced endothelial dysfunction (FMD 6.3±0.5 pre- vs 6.5±0.6 post IR + IPC, P >0.05 n = 10); Naloxone did not affect the protective effect of IPC against endothelial IR injury (FMD 6.1±0.4 pre- vs 6.5±0.6 post Naloxone + IPC, P >0.05 n = 10). The plasma β-EP concentrations remained unchanged during the IPC stimulus.

Conclusion: The protective effects of IPC were not abolished by Naloxone. Plasma β-EP concentrations did not change in response to the protective stimulus. Further studies are required.