Abstract: Abstract: Oxidative stress and calcium over loading are thought to be important mechanism of ischemia and reperfusion (I/R) injury and main target of prevention and cure on studies for I/R injury. However, so far, mechanism of I/R injury yet is not completely clear. Sulfur dioxide (SO2) is a common outdoor air pollutant and is associated with day to day changes in hospitalization rates for lung disease. Our group found that SO2 could relax vascular smooth. We presume SO2, especially; endogenous SO2 may have important significance in physiology and pathology in I/R injury. In this a study, we investigated the action of SO2 on I/R hearts of rats. Methods: Hearts of rat was divided in three groups, I/R group; SO2 group; and HDX group. The Langendorff-prepared rat hearts model was used. The heart was under ischemia for 2 hours under hypothermic (40C) subsequent reperfusion/rewarming for 60min. Heart function was monitored by MacLab system for data collection. Results: In SO2 group recovery of heart function（LVP, ±dp/dtmax, HR, CF）decreased compared with that of group of I/R (p<0.05 or p<0.01); In HDX group recovery of heart function（LVP, ±dp/dtmax, HR, CF）increased compared with that of group of I/R (p<0.05 or p<0.01); In SO2 group activity of lactate dehydrogenase (LDH), Creatinekinase (CK), glutamic oxaloacetic transaminase (GOT), and content of myohemoglobin (Mb) in coronary flow (CF); content of Malonedialdehyd (MDA) and conjugated diene (CD), and GOT activity in tissue of cardiac muscle increased compared with I/R group (p<0.05 or p<0.01). In HDX group activity of LDH, CK, GOT, and content of Mb in CF; content of MDA and CD, and GOT activity in tissue of cardiac muscle decreased compared with those of I/R group (p<0.05 or p<0.01). In SO2 group content of glutathione (GSH) decreased compared with I/R group (p<0.05); In HDX group content of GSH increased compared with that of I/R group (p<0.05). In SO2 group content superoxide anion (O2-.), and hydroxyl radical (.OH) were produced by tissue of cardiac muscle, content of hydrogen peroxide (H2O2) and activity of superoxide dimutase (SOD) in tissue of cardiac muscle did not change compared with those of I/R group (p>0.05); In HDX group O2-., .OH were generated by cardiac muscle tissue, content of H2O2 and SOD activity in cardiac muscle tissue did not differ from those of I/R group (p>0.05). Conclusions: (1) endogenous SO2 was involved in isolated heart I/R injury of rat, and this injury was aggravated by exogenesis SO2. (2) Endogenous SO2 produced by tissue possibly increased in isolated heart I/R model of rat. (3) The fact that SO2 damage cardiac muscle tissue was through at least partly through increasing lipid peroxide of cardiac muscle tissue. (4) The fact that SO2 increased lipid peroxide of cardiac muscle tissue was through at least partly through decreasing GSH produced by cardiac muscle.

Key words: heart, ischemia and reperfusion (I/R) injury, sulfur dioxide (SO2)