e0141 The effects and mechanisms between DIDS and EDRV on acute ischaemia-reperfusion injury myocardium

Aim To investigate the effects and Mechanisms of chloride channel inhibitor, 4, 4′- Diisothiocyanostilbene-2, 2′- disulfonic acid (DIDS) and free radical scavenger, Edaravone (EDRV) on myocardial ischaemia/reperfusion injury (I/RI)in vivo. Methods Male Sprague-Dawley rats, subjected to 30 min of myocardial ischaemia and 4 h of reperfusion, were divided into five groups: sham group, I/RI group, DIDS group, EDRV group and DIDS+EDRV group. Left ventricular systolic pressure (LVSP), The maximal first derivative of developed pressure (±dp/dtmax), Myocardial infarction size, serum creatine kinase (CK) activity, lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity, malondialdehyde (MDA) concentration, myocardial apoptotic index, reactive oxygen species (ROS) were detected. Results There were no statistical difference in heart rate in each animal suffering myocardial ischaemia/reperfusion compared with sham group (p>0.05, n=8). LVSP and ±dp/dt max were decreased during the period of myocardial ischaemia except sham but there was no statistical difference (p>0.05, n=8), However, following reperfusion, the data showed that DIDS and EDRV significantly improved myocardial function in I/RI rats (n=8, p 2− and OH·showed that DIDS reduces free radical weaker than EDRV (p Conclusion 1. DIDS and EDRV protect myocardium from MI/R injury via improving cardiac function, reducing infarct size and suppressing cardiomyocyte apoptosis; 2. The mechanisms of cardioprotective effects of DIDS and EDRV were involved in inhibition of ROS activity. The protective effect of combined administration can be further enhanced, suggesting DIDS protects ischaemia/reperfusion injury myocardium via other distinctive mechanisms except above.