Endogenous sulfur dioxide aggravates myocardial injury in isolated rat heart with ischemia and reperfusion.

BACKGROUND

Ischemia-reperfusion (I/R) injury is an important clinical problem. This article investigated the role of sulfur dioxide (SO2) in the regulation of cardiac function and in the pathogenesis of cardiac I/R injury in isolated rat heart.

METHODS

Rat hearts isolated on a Langendorff apparatus were divided into control, I/R, I/R+SO2, and I/R+hydroxamate groups. Hydroxamate is an inhibitor of SO2 synthetase. I/R treatment was ischemia for 2 hr in hypothermic solution (4 degrees C), then reperfusion/rewarming (37 degrees C) for 60 min. Cardiac function was monitored by MacLab analog to a digital converter. Determination of sulfite content involved reverse-phase high performance liquid chromatography with fluorescence detection. Myoglobin content of coronary perfusate was determined at 410 nm. Myocardial malondialdehyde (MDA) was determined by thiobarbituric acid method, and conjugated diene (CD) was extracted by chloroform. 5,50-Dithiobis-2-nitrobenzoic acid was used to determine glutathione (GSH).

RESULTS

The results showed that I/R treatment obviously increased myocardial sulfite content, and sulfite content of myocardium was negatively correlated with the recovery rate of left-ventricle developed pressure and positively correlated with the leakage of myoglobin. In postreperfusion, myocardial function recovery was decreased by SO2. During reperfusion, myocardium-released enzymes, MDA and CD level were increased but myocardial GSH content was depressed with the treatment of SO2 donor. Incubation of myocardial tissue with SO2 significantly increased MDA and CD generation.

CONCLUSIONS

Endogenous SO2 might be involved in the pathogenesis of myocardial I/R injury, and its mechanism might be associated with an increase in lipid peroxide level and a decrease in GSH generation.