心肌缺血再灌注损伤是围术期发生心血管事件的主要原因之一，而钙超载是缺血再灌注损伤的主要因素。CaMKII及RyR2等调节蛋白参与了此过程，且α2肾上腺素能受体参与了对心肌组织CaMKII磷酸化的调控。我们前期研究表明：高选择性α2肾上腺素能受体激动剂右美托咪定可提高心脏手术患者的生存率，减轻心肌缺血再灌注损伤，但其机制有待进一步探讨。为此，我们推测右美托咪定可能通过调控心肌CaMKII和RyR2的磷酸化，减轻心肌缺血再灌注后Ca2+超载，同时进一步通过调控CaMKII/HDAC/MEF-2信号通路，从而减轻心肌肥厚。为验证这一假说，我们通过细胞、离体和在体缺血再灌注模型，采用膜片钳、激光扫描共聚焦显微镜及Real-Time PCR、Western blot、RNA干扰等方法，从分子、细胞和整体来探讨右美托咪定对大鼠缺血再灌注损伤心肌钙循环的调控及机制，为围手术期心肌保护提供新的理论依据。

Myocardial ischemia-reperfusion injury is one of the main causes for perioperative cardiovascular events, and Ca2+ overload is a key factor accounting for the injury. Regulatory proteins including CaMKII and RyR2 function in this process, and α-2 adrenergic receptor is also responsible for the regulation of the CaMKII phosphorylation. Our previous studies demonstrated that the use of dexmedetomidine, a highly selective α-2 adrenergic receptor agonist, could attenuate myocardial ischemia-reperfusion injury and improve the outcomes of patients undergoing cardiac surgery. However, the underlying mechanism warrants further investigation. Therefore, we hypothesize that dexmedetomidine can reduce myocardial hypertrophy by regulation of CaMKII and RyR2 phosphorylation, alleviation of Ca2+ overload, and regulation of CaMKII/HDAC/MEF-2 signaling pathway. To test this hypothesis, we explore the effect and mechanism of dexmedetomidine on myocardial Ca2+ cycling in rats under in vivo and in vitro myocardial ischemia-reperfusion injury models, by using patch clamp recording, laser scanning confocal microscope, Real-Time PCR, Western blot, and siRNA under molecular, cellular and organ levels, in order to provide a novel theoretical basis for perioperative myocardial protection.