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目的 :观察远端器官缺血性预处理 (RPC)对非缺血心脏功能的影响 ,初步探讨 RPC的作用机制。方法 :19只成年绵羊麻醉后随机分为对照组 (n=9)及 RPC组 (n=10 )。测定基础状态 (BS1 )各参数后 ,RPC组动物经历 3次左侧股动脉阻断 5 min及再灌注 5 m in,第三次再灌注后 10 min测 RPC后 (BS2 )各参数。对照组动物不阻断股动脉 ,但于相应时间测定 BS1 及 BS2 各参数。结果 :对照组 BS1 及 BS2 各参数无显著变化。 RPC显著降低平均动脉压(MAP)、外周血管阻力 (SVR)及冠脉循环阻力 (CVR) (P<0 .0 5 ) ;轻度增加心排出量及冠脉血流量 (P>0 .0 5 )。但RPC对心率、左房压、每搏输出量、射血分数及每搏作功无显著影响。 BS2 时 RPC组左室收缩末期压 (L VESP)、左室压力上升及下降最大速率 (± dp/ dtmax)、动脉有效弹回性 (Effective arterial elastance,Ea)均显著低于对照组 (P<0 .0 5 ) ,而心脏收缩及舒张期左室容积下降及增加最大速率 (± dv/ dtmax)无显著变化。结论 :远端器官缺血性预处理降低动脉有效弹性及循环阻力、减弱心脏收缩性的同时 ,并不减弱反而轻度增强心脏泵血功能 ,提高了心肌收缩效率。
Objective: To observe the effect of remote organ ischemic preconditioning (RPC) on non-ischemic cardiac function and to explore the mechanism of action of RPC. Methods: Nineteen adult sheep were randomly divided into control group (n = 9) and RPC group (n = 10). After determining the basal state (BS1) parameters, the animals in the RPC group underwent 3 occlusion of the left femoral artery for 5 min and reperfusion for 5 min, and the parameters of BS2 after the third reperfusion were measured. Animals in the control group did not block the femoral artery, but the BS1 and BS2 parameters were measured at the corresponding time. Results: The parameters of BS1 and BS2 in control group showed no significant changes. RPC significantly reduced mean arterial pressure (MAP), peripheral vascular resistance (SVR) and coronary artery resistance (CVR) (P <0.05); slightly increased cardiac output and coronary blood flow (P> 5). However, RPC had no significant effect on heart rate, left atrial pressure, stroke volume, ejection fraction and stroke effort. In the BS2 group, L VESP, ± dp / dtmax, and Ea were significantly lower in the RPC group than those in the control group (P < 0.05), while there was no significant change in left ventricular volume and maximal rate of increase (± dv / dtmax) during systole and diastole. CONCLUSION: Ischemic preconditioning of distal organs can reduce the effective elasticity and circulatory resistance of arteries, weaken cardiac contractility, but not weaken but enhance cardiac pump function and improve myocardial contractile efficiency.