Abstract

Objective To investigate the effects of remifentanil on sepsis induced acute respiratory distress syndrome (ARDS) in rats. Methods A total of 40 SD rats were randomly divided into four groups: control group, ARDS group, remifentanil control group, and remifentanil group. ARDS model was induced by administering 7.5 mg/kg lipopolysaccharide (LPS) via vein in the ARDS group and remifentanil group, and rats in the control group and remifentanil control group were injected with the same volume of saline. Then the rats in the remifentanil control group and remifentanil group were subcutaneously treated with 0.04 μg/kg remifentanil 6 hours after LPS administration. All rats were sacrificed at 8 h after LPS administration. Right lung tissue were used to examine lung pathology changes, the myeloperoxidase (MPO), wet/dry (W/D) ratio, tumor necrosis factor-α(TNF-α), interleukin-1β (IL-1β) and IL-6 levels in left upper lung were examined and compared. Moreover, protein content and cell count in bronchoalveolar lavage fluid (BALF) were detected. Results A large number of inflammatory cells infiltration at 8 h after LPS administration in the ARDS group and remifentanil control group, and above pathology changes were significantly alleviated in the remifentanil group. The levels of MPO [(1.98 ± 0.14) U/g vs. (0.89 ± 0.12) U/g], W/D ratio [(8.51 ± 0.13) vs. (3.83 ± 0.08)], TNF-α [(1 141 ± 114) ng/L vs. (186 ± 8) ng/L], IL-1β [(1 866 ± 291) ng/L vs. (201 ± 30) ng/L], IL-6 [(528 ± 61) ng/L vs. (246 ± 35) ng/L], protein content [(0.96 ± 0.02)g/L vs. (0.29 ± 0.01) g/L] and cell count [(11.57 ± 1.04) × 108/ml vs. (1.39 ± 0.29) × 108/ml] in the ARDS group were higher than those in the control group (all P<0.05). In the remifentanil group, the MPO level, W/D ratio, TNF-α, IL-1β, IL-6, protein content and cell count were (1.01 ± 0.12)U/g, 4.05 ± 0.12, (573.8 ± 49.6) ng/L, (769.5 ± 49.8) ng/L, (365.5 ± 35.8) ng/L, (0.53 ± 0.02) g/L and (7.57 ± 0.66) × 108/ml, respectively. Above parameters were all lower than those in the ARDS group (all P<0.05). Conclusion Remifentanil could decrease the inflammation response and prevent the development of ARDS induced by LPS which plays a protective role in rats. Key words: Remifentanil; Lipopolysaccharide; Acute lung injury; Cytokines

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