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目的:探讨右美托咪啶预处理对离体大鼠心脏缺血再灌注损伤时左心室功能的影响。方法:雄性SD大鼠32只,建立langendorff离体心脏模型,随机分为四组,每组8只,正常对照组(NC组),缺血再灌注损伤组(IR组),缺血预适应组(IP组),右美托咪啶预处理组(DP组)。所有大鼠均缺血30min,再灌注120min。设定心脏稳定15min为基础值T0、缺血前即刻为T1、缺血30min为T2、再灌注15、45、90、120min分别为T3、T4、T5及T6。观察各组心肌缺血再灌注后不同时间点冠脉流出量(CF)、心率(HR)及左心室功能(LVDP和±dp/dtmax)。结果:与NC组相比,在T2、T3、T4、T5、T6时间点,其余各组CF和左心室功能均降低(P<0.05);与IR组相比,在T2、T3、T4、T5、T6时间点,IP组和DP组左心室功能均升高(P<0.05);与IR组和IP组相比,在T2时间点,DP组CF降低(P<0.05)。结论:右美托咪啶预处理可有效改善缺血再灌注损伤时下左心室功能,对离体心脏具有一定的保护作用,是否与α2-肾上腺素能受体介导有关的确切机制不是很清楚,有待进一步探讨。
Objective: To investigate the effect of dexmedetomidine preconditioning on left ventricular function in isolated rat heart during ischemia-reperfusion injury. Methods: Thirty-two male Sprague-Dawley rats were randomly divided into four groups (n = 8 each): normal control group (NC group), ischemia reperfusion injury group (IR group), ischemic preconditioning Group (IP group), dexmedetomidine pretreatment group (DP group). All rats were ischemia 30min, reperfusion 120min. Set the cardiac stability 15min based on the value of T0, immediately before ischemia as T1, ischemic 30min as T2, reperfusion 15,45,90,120 min were T3, T4, T5 and T6. Coronary flow volume (CF), heart rate (HR) and left ventricular function (LVDP and ± dp / dtmax) were observed at different time points after myocardial ischemia / reperfusion in each group. Results Compared with NC group, CF and left ventricular function decreased at T2, T3, T4, T5 and T6 time points (P <0.05). Compared with IR group, At T5 and T6, LV function in both IP and DP groups was significantly increased (P <0.05). Compared with IR and IP groups, CF decreased in DP group at T2 (P <0.05). Conclusion: Dexmedetomidine preconditioning can effectively improve left ventricular function during ischemia-reperfusion injury and has some protective effect on isolated heart. It is not clear whether the mechanism of dexmedetomidine is related to α2-adrenergic receptor-mediated mechanism , To be further explored.