大鼠离体心脏缺血-再灌注过程的功能变化

Change of Isolated Rat Heart Function during Ischemic-Reperfusion

目的建立大鼠离体心脏缺血-再灌注（I／R）损伤模型，观察I／R过程心脏舒缩功能与冠脉流量变化。方法大鼠离体心脏采用Langendorff法灌流，对照组（n=8）心脏连续灌流80min；I／R组（n=8）心脏缺血40min再灌注40min。实验过程实时动态检测心率（min^-1）、心肌收缩幅度（g）与最大收缩速度（dT／dtmax，g／ms）、最大舒张速度（-dT／dtmax，g／ms）、心肌静息张力（g）、冠脉流量（液滴，min^-1）。结果与对照组比较，I／R组心脏缺血后心搏停止，20min后心肌静息张力上升（P〈O．05）；再灌注后心肌张力仍高；心搏恢复但心率、心脏收缩幅度、最大收缩速度、最大舒张速度均降低（P〈0．05～0．001）；再复灌注初冠脉流量恢复正常，10min后呈下降性变化（P〈0．05～0．001）。结论大鼠离体心脏缺血40min再灌注40min导致I／R损伤，该模型制备及功能评价方法简便可靠。

Objective To establish ischemic-reperfusion（I/R） model and observe the functional change of the isolated rat heart during I/R process. Methods The isolated rat hearts perfused by Langendoff method was divided by two groups（n=8） ： the control group was continuously perfused for 80 min, the I/R group were non-perfused for 40 min and followed by reperfusion for 40 min. The heart rate （min^-1）, systolic amplitude（g）, systolic dT/dtmax（g/ms）, diastolic tension（g）, diastolic dT/dtm,, （g/ms） and coronary flow volume（drops/min^-1） were measured with BL-410E Bio-Function Experiment System. Results Compared with the control group, the systolic function of the I/R group was gradually arrested while the myocardium tension rose after non-perfusion（P〈0. 05）. The myocardium diastole tension keeps higher while the heart rate, systolic amplitude, systolic dT/dt diastolic dT/dtmax were decrease when reperfusion（P〈0.05-0. 001）. Coronary flow volume was recovery to normal at the beginning of reperfusion but continuously decrease during 40 min reperfusion（P〈 0. 05 -0. 001）. Conclusion It is convenient and available to prepare I/R injury model on the isolated rat heart by non-perfusion 40 min and reperfusion 40 min and evaluate the cardiac function during the myocardium I/R injury.