Abstract:

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.

Key words: Endogenous sulfur dioxide, Sepsis, Myocardic injury, Oxidant stress