Abstract

The purpose of this study was to investigate the effects of various remifentanil strategies (preconditioning, postconditioning, or continuous infusion) against myocardial ischemia-reperfusion injury. An in vitro experimental study using the Langendorff system. A university research laboratory. Male Sprague-Dawley rats (each n = 9). Five different remifentanil strategies were performed in isolated rat hearts as follows: remifentanil preconditioning (R-Pre), remifentanil postconditioning (R-Post), ischemic targeting remifentanil (R1), reperfusion targeting remifentanil (R2), or both ischemic and reperfusion targeting remifentanil (R3). Infarct size and cardiodynamics were compared. The infarct-risk volume ratio in groups R-Pre (13.7% ± 9.9%), R-Post (13.7% ± 12.3%), and R3 (12.6% ± 6.1%) were decreased significantly compared with the untreated control hearts (32.9% ± 11.1%, p &lt 0.01). There was no significant difference in the left ventricular-developed pressure (LVDP) recovery after reperfusion between the control (43.6% ± 14.5%) and R-Pre (34.8% ± 12.9%, p > 0.05) groups after reperfusion. However, the LVDP recovery in R-Post (21.6% ± 7.7%, p < 0.05), R1 (16.7% ± 19.8%, p < 0.01), R2 (22.2% ± 13.9%, p < 0.05), and R3 (16.2% ± 7.8%, p < 0.01) was decreased significantly compared with control hearts. There was no significant difference in the recovery of dP/dt(max) after reperfusion between the R-Pre (42.0% ± 16.9%) and control groups (39.0% ± 15.4%, p > 0.05), whereas the dP/dt(max) in R3 group (16.9% ± 9.0%) was decreased significantly compared with R-Pre (p < 0.05). Preconditioning or postconditioning by remifentanil and the continuous infusion of remifentanil effectively reduce myocardial infarction, whereas reperfusion targeting ischemic targeting or reperfusion targeting remifentanil does not. Remifentanil preconditioning better preserves myocardial function, especially LVDP, than other remifentanil strategies.

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