中文摘要：

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。

英文摘要：

Objective To investigate the effect of sulfur dioxide（SO2） preconditioning in physiological concentration on myocardium ischemia/reperfusion（I/R） injury and its mechanisms in rats by using 4-phenylbutyrate（4-PBA）.Methods Langendorff-prepared rat heart model was used.Hearts of rats were divided into 3 groups： I/R group,SO2＋I/R group and 4-PBA＋SO2＋I/R group.Heart function was monitored by Maclab system.Recording HR,left ventricular developed pressure（LVEDP）,＋dp/dtmax and-dp/dtmax as baseline of cardiac function before ischemia,and the cardiac function injury induced by ischemia reperfusion through recovery rate in the 3 groups were compared.Results Heart preconditioned with SO2 showed a higher recovery rate of heart function as compared with I/R group（Pa0.05）.The improvement of LVEDP and±dp/dtmax were significant.Heart perfused with 4-PBA before SO2 preconditioning showed a decreased recovery rate of heart function as compared with I/R＋SO2 group.After reperfusion for 30 min,the level of ＋dp/dtmax and-dp/dtmax were decreased..Conclusions SO2 preconditioning might protect against myocardium I/R injury via stimulating endoplasmic reticulum stress.4-PBA can reduce the protection of SO2 preconditioning on isolated myocardium I/R injury