Remifentanil limits infarct size but attenuates preconditioning-induced infarct limitation

Objectives We investigated the influence of the narcotic anesthetic remifentanil on irreversible myocardial ischemic injury. Methods New Zealand White rabbits were anesthetized with propofol (0.7-1.8 mg(.)kg(-1.)min(-1)) and then subjected to 30 min regional myocardial ischemia and 3 h reperfusion (CON). Some animals also underwent ischemic preconditioning, elicited by either one (IP1) or two (IP2) cycles of 5 min ischemia and 5 min reperfusion, and/or remifentanil, administered either as a transient infusion mimicking the preconditioning protocol (RP2, 10 mug(.)kg(-1.)min(-1)) or as a continuous infusion (R, 3-10 mug(.)kg(-1.)min(-1)). Rabbits were randomly assigned to experimental groups. Infarct size was assessed with tetrazolium. Results are reported as mean +/- SD. Results Non-preconditioned infarct size was similar to50% of the area-at-risk (49.6 +/- 20.1% CON). Both one and two cycles of ischemic preconditioning markedly reduced infarct size (49.6 20.1% CON versus 18.6 +/- 8.6% IP and versus 7.5 +/- 7.6% IP2; both p < 0.001). Preconditioning with remifentanil modestly reduced infarct size (49.6 +/-20.1% CON versus 29.3 +/- 8.5% RP2; p < 0.01). However, sustained administration of remifentanil did not provide protection (49.6 +/- 20.1% CON versus 43.9 +/- 16.2% R), and it attenuated the protection offered by preconditioning (49.6 +/- 20.1% CON versus 35.6 +/- 20.7% R+ IP1, p=NS; and versus 14.5 +/- 14.5% R+ IP2; p < 0.05). Conclusion Transient pre-ischemic administration of remifentanil modestly reduces infarct size in propofol-anesthetized rabbits, but continuous administration of remifentanil increases the threshold for ischemic preconditioning-induced infarct limitation. (C) 2004 Lippincott Williams Wilkins.