利多卡因对缺血再灌注离体大鼠心功能的影响

目的：探讨利多卡因对缺血再灌注离体大鼠心功能的影响及其可能机制。方法：40只健康成龄雌性Wistar大鼠，随机分为5组（n=8），建立Langendorff模型。缺血再灌注组（A）：灌注Krebs—Henseleit（K—H）缓冲液；利多卡因1mg／L组（B）：灌注含1mg／L利多卡因的K—H液；利多卡因2．5mg／L组（C）：灌注含2．5mg／L利多卡因K—H液；利多卡因5mg／L组（D）：灌注含5mg／L利多卡因的K—H液；利多卡因＋格列苯脲组（E）：灌注含2．5mg／L利多卡因和10Ixmol／L格列苯脲的K—H液。各组分别缺血前灌注相应灌流液20min，全心缺血30min，再灌注60min。记录缺血前5min及再灌注30min和60min的心率（HR）、左心室形成压（LVDP）、左室内压上升最大速率（＋dp／dtmax）、左室内压下降最大速率（-dp／dtmax）等心功能参数。结果：与A组比较，再灌注30min和60min时，C组的HR、LVDP、-＋dp／dtmax均升高（P〈0．05），B、D两组上述参数变化无统计学意义（P〉0．05）。与C组比较，再灌注30min和60min时，E组各项参数均降低（P〈0．05）。结论：含2．5mg／L利多卡因的K—H液可显著改善缺血再灌注离体大鼠心功能，部分机制可能与心肌细胞和线粒体ATP敏感性钾通道有关。

Effects of lidocaine on isolated rat heart undergoing ischemia-reperfusion injury

Objective： To investiagate the effects of lidocaine on isolated rat heart undergoing ischemia-reperfusion injury and its possible mechanisms. Methods： 40 healthy majoritied female Wistar rats were randomly divided into 5 groups （n=8 in each）,including ischemia-reperfusion group （A）, perfused with Krebs-Henseleit buffer（KHB）; lidocaine 1 mg/L group （B）, with lidocaine 1 mg/L in KHB; lidocaine 2.5 mg/L group（C）, with lidocaine 2.5 mg/L in KHB; lidocaine 5 mg/L group（D）, with lidocaine 5 mg/L in KHB and lidocaine ＋glibenclamide group （E） with lidocaine 2.5 mg/L and glibenclamide 10 μmol/L added in KHB. The isolated hearts were mounted on Langendorff apparatus. All of them were perfused with homologous solution for 20 rain, then subjected to 30 min global ischemia followed by 60 min reperfusion. Heart rate （HR）, left ventricular developed pressure （LVDP）, differential pressure timemaxium （＋dp/ dtmax, -dp/dtmax） were recorded at 5 min before ischemia as baseline, at 30 min and 60 min of reperfusion. Results： The HR, LVDP, ＋dp/dtmax at 30 min and 60 min of reperfusion in group C were higher （P〈0.05） than that of group A. The HR,LVDP,＋dp/dtmax at 30 min and 60 min of reperfusion were much lower （P〈 0.05） in group E than that of group C. Conclusion： Lidocaine 2.5mg/L in KHB can improve the isolated rat heart function, which undergoes ischemia-reperfusion injury and the possible mechanisms are related to affecting ATP-sensitive potassium channels（KATP channels） partly at least.