salicylates and Tachycardia--Ventricular

Recent studies have suggested the ability of salicylic acid (SA) to trap the hydroxyl radicals (.OH) generated in reperfused ischaemic myocardium. This study was designed to examine the effect of SA on reperfusion-induced arrhythmias and postischaemic ventricular dysfunction. Isolated rat hearts perfused by the Langendorff technique were preperfused with SA for 10 min. Hearts were then made ischaemic for 30 min, followed by 30 min of reperfusion. The left-ventricular contractile functions, including left-ventricular developed pressure (LVDP) and its first derivative (LV dp/dt), and creatine kinase (CK) release, were determined before and after ischaemia. Epicardial electrocardiograms (ECG) were also employed to analyse the incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF). SA improved LVDP and LV dp/dt, and reduced CK release, as compared to the control group (p < 0.05). The incidence of VT and VF during reperfusion was also significantly reduced by SA (p < 0.05). Analysis of tissue thiobarbituric acid-reactive products indicates that SA decreased oxidative stress during reperfusion. In conclusion, these results suggest that SA reduces ventricular dysfunction and attenuates ventricular arrhythmias by trapping OH radicals upon reperfusion in isolated rat hearts.

Topics: Animals; Anti-Arrhythmia Agents; Creatine Kinase; Electrocardiography; Free Radical Scavengers; Hydroxyl Radical; In Vitro Techniques; Male; Myocardial Ischemia; Rats; Rats, Sprague-Dawley; Salicylates; Salicylic Acid; Tachycardia, Ventricular; Thiobarbituric Acid Reactive Substances; Ventricular Fibrillation; Ventricular Function, Left; Ventricular Pressure