Abstract: AIM: To investigate if alfentanil protects the isolated rat heart against myocardial reperfusion injury andif the mechanism of this protection ismediated via opi-oid receptors and NO-dependent pathways.METHODS: Langendorff rat hearts were perfused at constant pressure with Kreb-Henseleit (K-H) buffer for 20 min and then were perfusedwith test solution:K-H buffer or K-H buffer containing alfentanil 50 μg·L^-1, alfentanil 100 μg·L^-1, naloxone 200 μg·L^-1, alfentanil 100 μg·L-1 +naloxone 200 μg·L^-1, L-NAME 100 μmol·L^-1 and alfentanil 100 μg·L^-1 +L-NAME 100 μmol·L^-1.After 10 min of this, the hearts were subjected to 25 min normothermic (37 ℃) global ischemia followed by 30 min reperfusion with the same test solution as before.To evaluate myocar-dial function, LVEDP, LVDP, ±dp/dt_max, HR and CF were measured at the 20th, 25 and 30th minute of perfu-sion and the 1st, 3rd, 5th, 10th, 20th and 30th minute of reperfusion.After experiment, the NOS and ATP con-tent of myocardium were assessed.RESULTS: Before is-chemia, alfentanil 100 μg·L^-1 decreased the HR at the 30th minute compared with the 20th minute(P<0.05). Treatment with 50 μg·L^-1 alfentanil and alfentanil 100 μg·L^-1 improved post-ischemic mechanical function assessed by LVEDP, LVDP and ±dp/dt max compared with controls after 30 min of reperfusion(P<0.05 or P <0.01).Furthermore, 100 μg·L^-1 alfentanil improved post-ischemic mechanical function better than 50 μg·L^-1 alfentanil indicated by lower LVEDP and higher-dp/ dt max (P<0.05).These effects were attenuated by 200 μg·L^-1 naloxone and 100 μmol·L^-1 L-NAME.CONCLUSION: Alfentanil have few inhibitive effects on the mechanical function of the non-ischemic hearts and have dose-depended protective effects against myocardial reperfusion injury by a mechanism mediated via opioid re-ceptors and NO-dependent pathways in rats.

Key words: alfentanil, naloxone, L-NAME, my-ocardial reperfusion injury