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Objective: In this study, sepsis induced by cecal ligation and puncture model of acute lung injury, sepsis dynamic observation of the early changes in alveolar macrophages and lung endothelial cell damage situation, and explore whether the two have some relevance and possible mechanisms. Methods: SD rats 66, male or female, were randomly divided into three groups: (1) normal control group (n = 6), animals were anesthetized, weighed, blood through the aorta, detected by enzyme-linked immunosorbent assay Serum E-selectin, tumor necrosis factor-α (TNF-α) levels. Rats were killed and the lungs, the alveoli repeatedly washed three times, bronchoalveolar lavage fluid, determined by enzyme-linked immunosorbent assay macrophage inflammatory protein-1α (MIP-1α) levels, to take a little mid-lung vascular tissues electron microscopy endothelial cells (VEC) and type Ⅱ alveolar epithelial cells (AT Ⅱ) injury, using electronic weighing scales lung wet weight, at 80 ℃ oven retained after 48h, weighed lung dry weight. And calculate the lung wet / dry weight (W / D), lung coefficient, lung water content; (2) sham group (n = 30), animals were anesthetized cecum underwent exploratory abdominal surgery closed, respectively, after 3h, 9h, 24h, 36h and 48h five point line with the normal control group of the same steps, each time point six rats; (3) sepsis group (n = 30), animal line cecal ligation and puncture (CLP) After 3h, 9h, 24h, 36h and 48h five point line with the normal control group of the same steps, each time point six rats. Results: 1. 3h after CLP sepsis in lavage fluid that elevated levels of MIP-1α, and the normal control group and sham operation group, the difference was statistically significant (p lt; 0.05), and the gradual rise high, peaked at 24h (1.45 ± 0.34 ng / ml), a decrease in the 36h time point performance, but still higher than the normal control group and sham operation group (p lt; 0.05). (2) the level of serum TNF-α was significantly higher than that in normal after CLP control group and the sham group (p lt; 0.01), peaked at 24h (390.94 ± 27.70 pg / ml), followed by a downward trend, but still significantly higher than the normal control group and sham operation group (p lt; 0.01). 3.CLP 3h postoperative serum E-selectin levels began to increase (0.26 ± 0.02ng/ml), significantly higher than the control group and the sham group (p lt; 0.05), peaked at 24h (0.40 ± 0.01ng / ml), followed by a downward trend, but still higher than the normal control group and sham operation group (p lt; 0.05). 4 lung wet / dry weight (W / D) values, lung coefficient, lung water content after CLP were significantly higher than in the control group (p lt; 0.05) and sham operation group (p lt; 0.05), with time, the ratio gradually increased, and at each time point were significantly higher than the control group (p lt; 0.01) with the sham group (p lt; 0.05). Above indicators in the sham group at all time points after surgery were significantly higher than the control group (p lt; 0.05), was statistically significant. 5 electron microscopy lung vascular endothelial cells (VEC) and type Ⅱ alveolar epithelial cells (AT Ⅱ) in the process of development of sepsis damage gradually increased, and in accordance with \Cell injury scores gradually increased over time. AT Ⅱ normal shape to maintain its normal function, this experiment AT Ⅱ gradual destruction of the normal form. 6 lavage fluid macrophage inflammatory protein-1α and serum E-selectin SPSS13.0 statistical analysis software package, there was a significant positive correlation, F = 5.557, P lt; 0.05, the correlation coefficient was 0.407, P lt; 0.01. the regression equation: y (MIP-1α) = 0.504 1.814x (E-selectin). Conclusions: In sepsis induced acute lung injury during alveolar macrophages may contribute to increase Large lung inflammatory injury, and high inflammation, increase pulmonary vascular permeability, helps the formation of pulmonary edema in acute lung injury induced sepsis play an important key. (2) the degree of aggregation of alveolar macrophages and vascular endothelial cell damage has a significant positive correlation, suggesting that alveolar macrophages and endothelial cells in the lung injury process may play an important role.
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