Dexmedetomidine attenuates acute kidney injury in children undergoing congenital heart surgery with cardiopulmonary bypass by inhibiting the TLR3/NF-κB signaling pathway

被引:1
|
作者
Xie, Yang [1 ,2 ]
Jiang, Wenqiang [2 ]
Cao, Jianfang [1 ]
Xie, Hong [1 ]
机构
[1] Soochow Univ, Affiliated Hosp 2, Dept Anesthesiol & Crit Care, 1055 Sanxiang Rd, Suzhou 215008, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Suzhou Hosp, Dept Anesthesiol, Suzhou Municipal Hosp, Suzhou, Jiangsu, Peoples R China
来源
关键词
Dexmedetomidine; cardiopulmonary bypass; acute kidney injury; NF-kappa B; CARDIAC-SURGERY; CASPASE-3; RATS;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Objective: To investigate the effect of dexmedetomidine (DMED) on acute kidney injury in children undergoing congenital heart surgery (CHS) with cardiopulmonary bypass (CPB). Methods: The children undergoing CHS with CPB were randomized to the control and the DMED groups. The children in the DMED group were injected with DMED (1 mu g/kg) followed by DMED infusion (0.5 mu g/kg/h) until 12 h after operation; the controls received normal saline. Markers were detected before operation (TO), 30 min after anesthesia induction (T1), and at 24 h, 48 h, and 72 h after operation (T2,T3, T4). Results: The heart rate and mean arterial pressure in the DMED group decreased at T1 and differed from controls at T1-T3 (all P<0.05). No intergroup differences were observed in the central venous pressure and caspase-3 level (all P>0.05). The DMED group had higher central venous pressure at T3 than at TO (P<0.05). At T2-T4, the DMED group had lower percentages of TLR3(+) cells than the controls (all P<0.05). In the DMED group, the percentagesof TLR3(+) cells decreased with time; whereas in the control group, the percentage increased with time (all P<0.05). Compared with the controls, the DMED group had lower levels of NF-kappa B and TLR3 at T2-T4, lower levels of sCr, IL-1 beta, and TNF-alpha at T3-T4, and lower incidence of AKI at T3 (all P <= 0.01). Conclusion: DMED can reduce the risk of AKI in children undergoing CHS with CPB, which may be because DMED can inhibit TLR3/NF-kappa B signaling and its downstream inflammatory mediators.
引用
收藏
页码:2763 / 2773
页数:11
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