Abstract: AIM:To investigate the protective effect of polydatin (PD) on calcium signals in thermally injured cardiomyocytes. METHODS: Twenty eight adult Sprague Dawley rats were randomly divided into four groups (seven rats/group): shamoperation group, thermal injury group, PD group and thermal injury+PD group. Polydatin (10 mg/kg) was given intravenously 5 min after operation. Twelve hours after thermal injury, single myocytes were isolated from ventricular free wall enzymatically and loaded with Ca2+ indicator fluo4 AM. Ca2+ sparks and transients were recorded. RESULTS: PD significantly improved left ventricular systolic pressure (LVSP), +dP/dtmax and dP/dtmax of thermal injury cardiomyocytes (P<0.01). Polydatin significantly increased thermal injury systolic Ca2+ transients by about 26% and myocyte contractility (P<0.01), restored sarcoplasmic reticulum Ca2+ content (P<0.01), inhibited thermal injuryinduced high frequency and the duration of calcium sparks (P<0.05). CONCLUSION: Polydatin has the capability of preventing SR leak and restoring intracellular Ca2+ homeostasis in thermal traumatized hearts and ameliorates thermally induced cardiac dysfunction, thus exerting strong therapeutic effect against burngenerated cardiac dysfunction.