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Chinese Journal of Critical Care Medicine(Electronic Edition) ›› 2021, Vol. 14 ›› Issue (01): 10-14. doi: 10.3877/cma.j.issn.1674-6880.2021.01.002

Special Issue:

• Immunosensescence and Sepsis • Previous Articles     Next Articles

Possible mechanism and dose correlation of dexmedetomidine in inhibiting inflammatory response in patients with sepsis

Dandan Gong1, Shuang Xu2, Xiaodong Jiang2,(), Jian Yu2   

  1. 1. Department of Cardiology, Dalian Municipal Central Hospital, Dalian 116033, China
    2. Department of Intensive Care Unit, the Second Hospital of Dalian Medical University, Dalian 116027, China
  • Received:2020-06-29 Online:2021-02-28 Published:2021-04-25
  • Contact: Xiaodong Jiang

Abstract:

Objective

To investigate the possible mechanism and dose correlation of dexmedetomidine sedation in treating the inflammatory response of patients with sepsis.

Methods

From November 2017 to October 2018, 75 patients with sepsis requiring mechanical ventilation were selected from the ICU of the Second Hospital of Dalian Medical University. They were divided into a low dose group, a high dose group and a control group, with 25 patients in each group. Patients in the low dose group and high dose group were initially given 0.5 μg/kg and 1.5 μg/kg of dexmedetomidine respectively, and continued sedation treatment with 0.2 μg·kg-1·h-1 and 0.6 μg·kg-1·h-1 of dexmedetomidine. Patients in the control group were treated with 1 mg/kg of propofol within 15 min, and then sustained sedation with doses of 1~3 mg·kg-1·h-1. The general data of all patients were recorded, and the expression levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and nuclear factor-kappa B (NF-κB) at pre-medication (T0), 12 h after medication (T1) and 24 h after medication (T2) were measured by enzyme-linked immunosorbent assay in these three groups. Pearson correlation analysis was used to explore the correlation between NF-κB and TNF-α, IL-6.

Results

The expression levels of TNF-α, IL-6 and NF-κB at T0, T1 and T2 were statistically significantly different in the three groups (F=3.501, 3.258, 12.218; all P < 0.05). A further pairwise comparison found that at T1, the expression levels of TNF-α [(14 ± 6), (29 ± 18), (27 ± 16) ng/L] and IL-6 [(49 ± 26), (178 ± 110), (180 ± 115) ng/L] in the high dose group were significantly lower than those in the low dose group and control group, and the expression level of NF-κB [(2.84 ± 0.71) μg/L vs. (3.89±0.51) μg/L] in the high dose group was significantly lower than that in the control group (all P < 0.05). At T2, the expression level of TNF-α [(7 ± 5) ng/L vs. (19 ± 9) ng/L] in the high dose group was significantly lower than that in the control group, and the expression levels of IL-6 [(19 ± 11), (91 ± 53), (96 ± 57) ng/L] and NF-κB [(1.91 ± 0.94), (2.67 ± 0.70), (3.25 ± 0.58) μg/L] in the high dose group were significantly lower than those in the low dose group and control group (all P < 0.05). No significant difference was noted in the expression levels of TNF-α, IL-6 and NF-κB at T1 and T2 between the low dose group and control group (all P > 0.05). Pearson correlation analysis showed that NF-κB was positively correlated with serum TNF-α (r=0.456, P < 0.001) and IL-6 (r=0.309, P=0.007).

Conclusion

Dexmedetomidine can reduce the levels of TNF-α and IL-6 in patients with sepsis by inhibiting NF-κB in the cholinergic anti-inflammatory pathway, and its anti-inflammatory effect is positively correlated with its dose.

Key words: Dexmedetomidine, Sepsis, Mechanical ventilation, Analgesia and sedation, Inflammatory factor

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