中文摘要：

目的研究利多卡因对七氟烷后处理心肌保护作用的影响，并探讨其可能的机制。方法采用Langendorff装置平衡灌注20min后，全心停灌40min，再灌注120min，建立雄性Sprague-Dawley大鼠离体心脏缺血，再灌注（ischemia／reperfusion，I／R）模型。采用随机数字表法将大鼠心脏随机分为7组（每组6只）：假手术（Sham）组、I／R组、I／R＋20mg／L利多卡因（I／R＋Lid-20）组、七氟烷后处理sevofluranepostconditioning，SPC）组、七氟烷后处理＋2、10mg／L或20mg／L利多卡因（SPC＋Lid-2、SPC＋Lid．10、SPC＋Lid-20）组。连续监测左室发展压（1eftventriculardevelopingpressure，LVDP）、舒张末压（1eftventricularend-diastolicpressure，LVEDP）、心率（heartrate，HR）、左室内压上升／下降最大速率（maximalrise／fallrateofleftventricularpressure，＋dp／dtmax）以及冠脉流量（coronaryarteryflow，CF）。于再灌注5min和10min时，收集冠脉流出液测定乳酸脱氢酶（1actatedehydrogenase，LDH）和肌酸激酶（creatinekinase，CK）的活性。于再灌注末测定心肌梗死面积及相关蛋白的表达。结果与I／R组比较，SPC组、SPC＋Lid-2组以及SPC＋Lid-10组的LVDP、dp／dt。和cF均明显升高，LVEDP、LDH和CK活性、心肌梗死面积[（23．9±1．4）％，（20．5±1-3）％，（24．7±2．1）％vs（47．9±3.3）％]均明显降低（尸〈0．05）；而I／R＋Hd-20组、SPC＋Lid-20组的各指标与I／R组比较，差异无统计学意义（P〉0．05）；SPC纽上调了心肌磷酸化的Akt（phosphoralated-Akt，p-Akt）、磷酸化的细胞外信号调节激酶112（phosphoralated-extracellularregulat．edkinasel／2，P-Erkl／2）以及Bcl-2的表达（P〈0．05VSI／R组），而20mg／L的利多卡因抑制了SPC对心肌Bcl-2表达的上调作用。结论20mg／L的利多卡因取消了SPC的心肌保护作用，此效应可能与抑制Bcl-2蛋白表达有关。

英文摘要：

Objective To investigate the effects of lidocaine on sevoflurane postconditioning-induced cardioprotection and detect its potential mechanism. Methods Chose healthy adult male Sprague-Dawley rats. Their hearts were excised and per/used in a Langendorff apparatus. After 20 min of equilibration, the hearts subjected to 40 rain of ischemia followed by 120 rain of reperfusion, then randomly divided into the following seven groups （n=6 each）： Sham-operation （Sham）, ischemiaJreperfusion （I/R）, isehemia/reperfusion and 20 mg/L lidocaine（l/R＋Lid-20）, sevoflurane posteonditioning（SPC）, SPC and 2, 10 or 20 mg/L lidocaine （SPC＋Lid-2, SPC＋Lid-10, SPC＋Lid-20）. After 20 rain of equilibration, the hearts subjected to 40 rain of ischemia followed by 120 rain of reperfusion, left ventricular developing pressure （LVDP）, ]eft ventricular end-diastolic pressure （LVEDP）, heart rate （HR）, maximal rise/fall rate of left ventrieular pressure （＋dp/dtm=） and coronary artery flow（CF） were recorded continuously. Coronary effluent was collected at 5 and 10 min of reper/usion for determination of lactate dehydrogenase （LDH） and creatine kinase （CK） activities. Myocardial tissues were obtained at the end of reperfusion for determination of infarct size （IS） and related proteins. Results The LVDP, dp/dtmax , CF were significantly higher and LVEDP, LDH and CK activities, IS [ （23.9±1.4）%, （20.5±1.3）%, （24.7±2.1）% vs （47.9±3.3）%] were markedly lower in the SPC, SPC＋Lid-2, SPC＋Lid-10 groups than in the I/R group at all points of reperfusion （P〈0.05）; Compared with group I/R, all the measures were not significantly different in the I/R＋Lid-20 and SPC＋Lid-20 groups （P〉0.05）;The SPC group increased the expression of p-Akt, p-Erkl/2 and Bcl-2, but 20 mg/L lidocaine abolished the increased expression of Bc1-2 induced by SPC. Conclusions 20 mg/L lidocaine inhibits the protective effect induced by SPC and inhibition of Bc1-2 expression may be invol