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目的探讨生理水平的二氧化硫(SO2)预处理对大鼠离体心肌缺血再灌注(I/R)损伤的保护作用,通过使用内质网应激抑制剂4-苯基丁酸(4-PBA)来探讨SO2预处理的作用机制。方法应用Langendorff技术建立大鼠离体心脏灌注模型。将21只Wistar大鼠离体心脏随机分为3组:I/R组、SO2+I/R组及4-PBA+SO2+I/R组。通过Maclab采集系统监测心脏功能。记录缺血前30 min心功能指标,以缺血前离体心脏心率、左心室内压差、左心室内最大上升速率及最大下降速率为基础值,比较再灌注期间各组离体心脏各项心功能指标恢复率变化。结果 I/R可引起再灌注期间大鼠离体心脏心功能恢复率显著下降。经5μmol.L-1SO2预处理后,相对于I/R组,再灌注期间大鼠离体心脏的各项心功能恢复率有不同程度的改善(Pa<0.05),其中以左心室内压差、左心室内最大上升速率及最大下降速率改善最为明显。预先给予4-PBA持续灌流后,SO2预处理对大鼠I/R损伤的保护作用有不同程度的下降。相对于单纯SO2预处理组,4-PBA+SO2+I/R组再灌注30 min后左心室内最大上升速率及最大下降速率恢复显著下降。结论 SO2可能通过激活内质网应激反应发挥对大鼠I/R损伤的保护作用,4-PBA可部分逆转SO2预处理对于心脏I/R损伤的保护作用。
Objective To investigate the protective effects of physiological level of SO2 preconditioning on isolated rat myocardial ischemia-reperfusion (I / R) injury. By using endoplasmic reticulum stress inhibitor 4-PBA ) To explore the mechanism of SO2 pretreatment. Methods The isolated rat heart perfusion model was established by Langendorff technique. Twenty-one Wistar rats were randomly divided into three groups: I / R group, SO2 + I / R group and 4-PBA + SO2 + I / R group. Monitor heart function with Maclab acquisition system. Thirty minutes before ischemia, the cardiac function was recorded. Based on the pre-ischemic heart rate, left ventricular pressure difference, maximum rate of left ventricular ascending and maximum rate of descent, the changes of isolated heart Heart function index recovery rate changes. Results I / R caused a significant decrease of cardiac function recovery rate of rat isolated heart during reperfusion. After pretreatment with 5μmol.L-1SO2, cardiac function recovery rates of isolated rat hearts were improved to some extent (P <0.05) compared with I / R group. The left ventricular pressure difference , The largest rate of left ventricular ascending and maximum rate of decline to improve the most obvious. Pretreatment with 4-PBA continued perfusion, SO2 pretreatment on I / R injury in rats with varying degrees of decline. Compared with pure SO2 pretreatment group, the maximal rate of rise and the maximum rate of decrease of left ventricle in 4-PBA + SO2 + I / R group decreased significantly after 30 min reperfusion. Conclusion SO2 may play a protective role in I / R injury through activation of endoplasmic reticulum stress. 4-PBA may partially reverse the protective effect of SO2 preconditioning on cardiac I / R injury.