Fentanyl reduces infarction but not stunning via delta-opioid receptors and protein kinase C in rats

Langendorff rat hearts were used (i) to examine whether fentanyl reduces st unning, infarction or both, and (ii) to investigate if this protection is m ediated by delta-opioid receptors and/or protein kinase C (PKC). in the stu nning study, hearts were subjected to global ischaemia (20 min) and reperfu sion. This did not produce infarction. Postischaemic mechanical function wa s measured in hearts treated with or without fentanyl (740 nM). Fentanyl di d not affect postischaemic mechanical function. In the infarction study, th e left anterior descending coronary artery was occluded for 35 min and infa rct size was assessed by triphenyltetrazolium chloride staining. Hearts in the control group exhibited an infarct zone/area at risk (IIR) of 39 (SEM 5 )%, whereas the I/R for the fentanyl group was 13 (2)%. When the hearts wer e treated with a delta-opioid receptor antagonist (naltrindole I nM) or a P KC inhibitor (chelerythrine 2 mu M), the effect of fentanyl was abolished, with IIR of 37 (1) and 36 (2)% respectively. In our model, we conclude that fentanyl protects against infarction but not against stunning, and that th e limitation of ischaemic injury is mediated by both delta-opioid receptors and PKC.