N-acetylcysteine and atorvastatin alleviates lung injury due to ischemia-reperfusion injury in rats

Figures

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  Fig. 1. Vein gas exchange levels at the end of the experimental period. Data are presented as medians with total range. Sham (n = 6), no injury; IR (n = 6), no pretreatment; ATOR (n = 6), atorvastatin administered through gavage; NAC (n = 6), N-acetylcysteine administered intraperitoneally; and A + N (n = 6), both drugs administered. *p < 0.05 vs IR group. Vein gas pH (A); vein gas BE (B); vein gas PvCO2 (C); vein gas HCO3– levels (D). A + N, atorvastatin + N-acetylcysteine; ATOR, atorvastatin; BE, base excess; HCO3-, bicarbonate; IR, ischemia-reperfusion; NAC, N-acetylcysteine; PvCO2, partial pressure of carbon dioxide; SHAM, sham treatment.

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  Fig. 2. Lung injury evaluation. Representative pulmonary histological photographs of the five experimental groups. Increased leukocyte infiltration, edema, and hemorrhage were noted after IR (arrows). Pretreatment decreased the lung inflammatory infiltration. The sums of lung injury scores are presented as medians with total range. *p < 0.05 vs IR group. A + N, atorvastatin + N-acetylcysteine; ATOR, atorvastatin; IR, ischemia-reperfusion; NAC, N-acetylcysteine; SHAM, sham treatment.

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  Fig. 3. Lung wet-to-dry weight ratio. Edema formation (wet/dry weight) in lung tissue increased following mesenteric ischemia-reperfusion. Data are presented as medians with total range. *p < 0.05 vs IR group. A + N, atorvastatin + N-acetylcysteine; ATOR, atorvastatin; IR, ischemia-reperfusion; NAC, N-acetylcysteine; SHAM, sham treatment.

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  Fig. 4. Lung tissue cytokine levels. Lung tissue levels of TNF-α (left), IL-1β (middle), and IL-6 (right) increased following mesenteric ischemia-reperfusion. Data are presented as medians with total range. *p < 0.05 vs IR group. A + N, atorvastatin + N-acetylcysteine; ATOR, atorvastatin; IL, interleukin; IR, ischemia-reperfusion; NAC, N-acetylcysteine; SHAM, sham treatment; TNF-α, tumor necrosis factor-α.