[Regulative effects of endogenous sulfur dioxide on oxidant stress in myocardium of rat with sepsis].

OBJECTIVE

To explore the modulating effect of endogenous sulfur dioxide (SO2) on the ba-lance of oxidation/reduction in the cecal-ligation-and-puncture-induced septic rat myocardium.

METHODS

Forty male Sprague Dawley rats were randomized into control group, SO2group, sepsis group and sepsis + SO2group. The levels of procalcitonin (PCT), creatine kinase isoenzyme (CK-MB), cardiac troponin Ⅰ (cTn Ⅰ) and fatty acid binding protein (FABP) in plasma in each group of the rats were measured; The level of hydrogen peroxide (H2O2), level of nitric oxide (NO), activity of myeloperoxidase (MPO), activity of hydroxyl free radical (·OH) and level of malondialdehyde (MDA) in myocardial tissue were measured; Total antioxidant capacity (T-AOC), activity of catalase (CAT), level of cytochrome oxidase (CO), level of glutathione (GSH), level of glutathione oxidase (GSH-px) and activity of superoxide dismutase (SOD) in myocardial tissue were measured.

RESULTS

The level of PCT in plasma in the rats with sepsis increased from (0.93±0.26) μg/L to (2.45±0.52) μg/L (P < 0.01), and decreased to (1.58±0.36) μg/L after the intervention of sulfur dioxide donor (P < 0.01). In sepsis, the plasma CK-MB, cTn Ⅰ and FABP levels in the rats increased respectively from (14.46±6.48) μg/L, (151.25±30.14) ng/L and (2.72±0.65) μg/L to (23.72±7.72) μg/L, (272.78±52.70) ng/L and (5.22±1.01) μg/L (P all < 0.01), and decreased to (16.74±3.63) μg/L, (184.86±37.72) μg/L and (3.31±0.84) μg/L (all P < 0.05) after the intervention of sulfur dioxide donor. The level of H2O2, level of NO, activity of MPO, activity of ·OH and level of MDA in myocardial tissue in the rats with sepsis increased respectively from (67.26±8.77) mmol/g, (38.39±6.93) μmol/g, (358.25±68.12) U/g, (648.42±93.69) U/ mg and (4.55±0.96) μmol/g to (111.45±17.35) mmol/g, (51.04±5.91) μmol/g, (465.88±76.76) U/g, (873.75±123.47) U/mg and (7.25±0.86) μmol/g (all P < 0.01), and decreased respectively to (75.99±10.52) mmol/g, (39.39±7.80) μmol/g, (393.17±51.5) U/g, (710.54±106.33) U/mg and (5.16±0.65) μmol/g after the intervention of the sulfur dioxide donor (all P < 0.05). The activity of T-AOC, activity of CAT, level of CO, level of GSH, level of GSH-px and activity of SOD in myocardial tissue in the rats with sepsis increased respectively from (2.07±0.37) U/mg, (169.25±36.86) U/g, (1.35±0.32) μmol/g, (103.51±16.62) μmol/g, (38.40±7.97) μmol/g and (38.50±8.30) U/mg to (1.42±0.39) U/mg, (98.44±26.56) U/g, (0.96±0.21) μmol/g, (68.05±7.35) μmol/ g, (23.83±5.04) μmol/g and (23.11±4.63) U/mg (P all < 0.01), and increased respectively to (1.83±0.37) U/mg, (146.14±31.63) U/g, (1.28±0.20) μmol/g, (92.10±11.84) μmol/g, (37.16±3.01) μmol/g and (37.29±2.62) U/mg (P all < 0.05) after the intervention of the sulfur dioxide donor.

CONCLUSION

Endogenous SO2 can protect rat myocardium in sepsis by modulating the ba-lance of oxidation and reduction.