乌司他丁对脓毒症急性肺损伤的保护作用研究
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摘要
目的:观察乌司他丁对脓毒症急性肺损伤的保护作用,并探讨其可能的作用机制。方法:收集2017-04—2018-05期间接受治疗的脓毒症伴发急性肺损伤患者124例,按照患者入院顺序随机分为观察组和对照组,每组62例。对照组常规治疗,观察组在常规治疗基础上加用乌司他丁20万单位/d,静脉滴注。ELISA法检测p65、TNF-α、IL-6表达。结果:治疗前,两组p65、TNF-α和IL-6水平比较,差异无统计学意义(P>0.05)。治疗后,观察组p65、TNF-α和IL-6水平分别为(24.36±4.33)μg/L、(31.38±6.06)μg/L和(18.52±3.38)μg/L,显著低于对照组的(38.24±7.25)μg/L、(46.36±7.54)μg/L和(32.16±5.23)μg/L(P<0.01)。治疗前,两组PaO_2和PaO_2/FiO_2比较,差异无统计学意义(P>0.05)。治疗后,观察组PaO_2和PaO_2/FiO_2分别为(80.23±12.63)mmHg、(387.82±62.33)mmHg,均显著高于对照组的(67.28±10.26)mmHg和(322.18±54.27)mm-Hg,差异有统计学意义(P<0.05)。观察组有效率为90.3%(56/62),显著高于对照组的75.8%(47/62)。结论:乌司他丁可以抑制脓毒症急性肺损伤患者炎症反应,改善患者肺功能,临床疗效显著。
Objective:To observe the protective effects of ulinastatin on sepsis induced acute lung injury.Method:124 sepsis induced acute lung injury patients were divided into control group(n=62)and observation group(n=62).The control group was given conventional treatment,and the observation group on the base of control group was given ulinastatin.p65,TNF-α,IL-6 were detected by ELISA analysis.Result:There was no significant difference in the levels of p65,TNF-and IL-6 between the two groups before treatment(P>0.05).After treatment,the p65,TNF-α,IL-6 in observation group was 24.36±4.33μg/L,31.38±6.06μg/L,and 18.52±3.38μg/L,which were significantly lower than those in control group(38.24±7.25,46.36±7.54 and 32.16±5.23μg/L,P <0.01).There was no significant difference of PaO_2 and PaO_2/FiO_2 between the two groups before treatment(P>0.05).After treatment,the PaO_2 and PaO_2/FiO_2 in observation group were(80.23±12.63)mmHg and(387.82±62.33)mmHg,which were significantly higher than those in control group(67.28±10.26 and 322.18±54.27 mmHg),P<0.05).The effective rate of observation group was 90.3%(56/62),which was significantly higher than that in control group(75.8%)(47/62)(P<0.05).Conclusion:Ulinastatin can inhibit the inflammation reaction in septic patients with acute lung injury to improve lung function.
Objective:To observe the protective effects of ulinastatin on sepsis induced acute lung injury.Method:124 sepsis induced acute lung injury patients were divided into control group(n=62)and observation group(n=62).The control group was given conventional treatment,and the observation group on the base of control group was given ulinastatin.p65,TNF-α,IL-6 were detected by ELISA analysis.Result:There was no significant difference in the levels of p65,TNF-and IL-6 between the two groups before treatment(P>0.05).After treatment,the p65,TNF-α,IL-6 in observation group was 24.36±4.33μg/L,31.38±6.06μg/L,and 18.52±3.38μg/L,which were significantly lower than those in control group(38.24±7.25,46.36±7.54 and 32.16±5.23μg/L,P <0.01).There was no significant difference of PaO_2 and PaO_2/FiO_2 between the two groups before treatment(P>0.05).After treatment,the PaO_2 and PaO_2/FiO_2 in observation group were(80.23±12.63)mmHg and(387.82±62.33)mmHg,which were significantly higher than those in control group(67.28±10.26 and 322.18±54.27 mmHg),P<0.05).The effective rate of observation group was 90.3%(56/62),which was significantly higher than that in control group(75.8%)(47/62)(P<0.05).Conclusion:Ulinastatin can inhibit the inflammation reaction in septic patients with acute lung injury to improve lung function.
引文
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[11]张慧慧,蔡国龙,胡才宝,等.乌司他丁对脓毒症大鼠急性肺损伤的保护作用及其机制研究[J].中华危重症医学杂志(电子版),2017,10(3):153-158.
[2]唐甜,谭利平.炎症反应在脓毒症ARDS发病机制中的作用[J].重庆医学,2017,46(15):2146-2149.
[3]Xu C,Guo Z,Zhao C,et al.Potential mechanism and drug candidates for sepsis-induced acute lung injury[J].Exp Ther Med,2018,15(6):4689-4696.
[4]孙小聪,佟琳,伍海斌,等.乌司他丁对急性肺损伤大鼠肺组织MMP-2、MMP-9表达的影响[J].四川医学,2017,38(2):140-143.
[5]Chvojka J,Matejovi CM.International guidelines for management of severe sepsis and septic shock 2012-comment[J].Vnitr Lek,2014,60(1):59-67.
[6]中华医学会呼吸病学分会.ALI/急性呼吸窘迫综合征的诊断标准(草案)[J].中华结核和呼吸杂志,2000,23(4):230-241.
[7]梁久红,邹子俊.低分子肝素治疗脓毒症急性肺损伤/急性呼吸窘迫综合征的疗效观察[J].临床医学工程,2016,23(8):1029-1030.
[8]谢敏崇,杜剑文,张海天,等.脓毒症继发急性肺损伤患者肺组织和血清细胞因子变化及临床意义[J].中华实用诊断与治疗杂志,2018,32(4):344-346.
[9]施荣,熊旭东,王倩.TRAF6-NF-κB/p38 MAPK通路活性在脓毒症致急性肺损伤中肺泡巨噬细胞过度极化的作用及炎调方干预的可能性探讨[J].临床急诊杂志,2018,19(1):37-39.
[10]Xu J,Lu C,Liu Z,et al.Schizandrin B protects LPS-induced sepsis via TLR4/NF-κB/MyD88 signaling pathway[J].Am J Transl Res,2018,10(4):1155-1163.
[11]张慧慧,蔡国龙,胡才宝,等.乌司他丁对脓毒症大鼠急性肺损伤的保护作用及其机制研究[J].中华危重症医学杂志(电子版),2017,10(3):153-158.