| Popis: |
To investigate the mechanisms of protective effects of dexmedetomidine on lungs in patients of sepsis complicated with acute respiratory distress syndrome (ARDS).The adult patients with sepsis complicated with ARDS, the oxygenation index (PaOThere were no significant changes for inflammatory factors in serum, and inflammatory signaling proteins and anti-apoptotic signaling proteins in alveolar exfoliated cells in no sedation group. The levels of IL-6 and TNF-α in serum and the expressions of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and phosphorylated c-Jun N-terminal kinase (p-JNK) in alveolar cells in propofol group and dexmedetomidine group were all significantly reduced after sedation, moreover, it was more significantly in the dexmedetomidine group compared with propofol group [48 hours: TNF-α (ng/L) was 153.76±29.16 vs. 179.82±30.28; 72 hours: IL-6 (ng/L) was 272.18±42.76 vs. 304.49±44.93, TNF-α (ng/L) was 102.18±30.25 vs. 140.28±28.92, TLR4 (IA value) was 0.288±0.034 vs. 0.648±0.029, MyD88 (IA value): 0.356±0.030 vs. 0.752±0.044, p-JNK (IA value): 0.256±0.027 vs. 0.303±0.034, all P0.05]. The expression of p-Akt in alveolar cells in propofol group and dexmedetomidine group was all significant increased after sedation, moreover, it was more significantly in the dexmedetomidine group compared with propofol group (IA value: 1.032±0.030 vs. 0.743±0.028, P0.05).Dexmedetomidine exerts the protective effects on lungs in patients of sepsis complicated with ARDS through the TLR4-MyD88-JNK signaling pathway. |
