目的：观察乌司他丁预处理对新肝期亲体肝移植术患儿心肌损伤的影响，并探讨其可能机制。方法择期行亲体肝移植术患儿30例，随机分为观察组和对照组各15例。观察组将2万U／kg乌司他丁用生理盐水稀释至1万U／mL，分别于切皮前即刻和门静脉开放前5 min各使用1／2剂量；对照组以等容量生理盐水代替。分别于切皮前即刻（ T0）、无肝期30 min（ T1）、新肝期3 h（ T2）和术毕（ T3）采集中心静脉血，采用Access2电化学发光仪检测血清心肌肌钙蛋白I（cTnI）、肌酸激酶同工酶（CK-MB），LX-20型全自动生化分析仪检测乳酸脱氢酶（LDH）活性，ELISA法检测血清肿瘤坏死因子α（TNF-α）、IL-6、IL-18。结果观察组T0～T3时点cTnI水平分别为（0．043±0．023）、（0．048±0．025）、（0．205±0．055）、（0．195±0．057）μg／L，CK-MB水平分别为（1．4±0．4）、（1．7±0．6）、（3．4±1．1）、（4．1±1．5）μg／L，LDH活性分别为（225±78）、（267±53）、（280±45）、（446±135）IU／L；对照组T0～T3时点cTnI水平分别为（0．046±0．027）、（0．051±0．027）、（0．378±0．084）、（0．326±0．082）μg／L，CK-MB水平分别为（1．6±0．5）、（1．9±0．5）、（4．2±0．8）、（5．3±1．7）μg／L，LDH活性分别为（254±85）、（275±75）、（339±87）、（577±156）IU／L；两组T2、T3时点分别与同组T0时点比较，P＜0．05或0．01；观察组T2、T3时点cTnI、CK-MB水平及LDH活性与对照组比较，P＜0．05或0．01。观察组T0～T3时点TNF-α水平分别为（34±10）、（38±11）、（142±45）、（121±41）pg／mL，IL-6水平分别为（65±21）、（70±24）、（85±23）、（102±33）pg／mL，IL-18水平分别为（16±4）、（18±6）、（60±21）、（114±43） pg／mL；对照组T0～T3时点TNF-α水平分别为（35±11）、（43±12）、（186±62）、（163±57）pg／mL，IL-6水平分别为（72±15）、（82±23）、（113±42）、（171±56）pg／mL，IL-18水平分别为（17±5）、（20±7）、（78±23）、（153±51）pg／mL；两组T2、T3时点分别与同组T0时点比较，P＜0．05或0．01；观察组T2、T3时点TNF-α、IL-6、IL-18水平与对照组比较，P＜0．05或0．01。结论乌司他丁预处理可在一定程度上减轻新肝期亲体肝移植术患儿心肌损伤，其机制可能与抑制炎症因子的过度释放有关。%Objective To investigate the effect of ulinastatin preconditioning on myocardial injury of pediatric patients undergoing living related liver transplantation ( LRLT) during neohepatic stage and its mechanism.Methods Thirty chil-dren, scheduled for LRLT, were randomly divided into two groups (n=15):the observation group and the control group. Ulinastatin 20 000 U/kg was diluted into 10 000 U/mL with normal saline and it was then injected intravenously in 2 parts (1/2 was injected before skin incision;1/2 at 5 min before portal vein declamping) in the observation group.In the con-trol group, the equal volume of normal saline was given instead of ulinastatin.Blood samples were taken from the central vein before skin incision ( T0 , baseline) , at 30 min after anhepatic phase ( T1 ) , 3 h of neohepatic stage ( T2 ) and the end of surgery ( T3 ) for the determination.The Access2 electrochemiluminescence instrument was used to detect serum cardiac troponin I ( cTnI) and creatine kinase isoenzyme ( CK-MB) concentrations.LX-20 type full automatic biochemical analyzer was used to measure the lactate dehydrogenase ( LDH) activity.ELISA method was used to detect the levels of serum TNF-α, IL-6 and IL-18.Results The serum concentrations of cTnI were (0.043 ±0.023), (0.048 ±0.025), (0.205 ± 0.055) and (0.195 ±0.057) μg/L, the serum CK-MB concentrations were (1.4 ±0.4), (1.7 ±0.6), (3.4 ±1.1) and (4.1 ±1.5) μg/L, and the LDH activities were (225 ±78), (267 ±53), (280 ±45) and (446 ±135) IU/L at T0-3 in the observation group.The serum cTnI concentrations were (0.046 ±0.027), (0.051 ±0.027), (0.378 ± 0.084), (0.326 ±0.082) μg/L, the serum CK-MB concentrations were (1.6 ±0.5), (1.9 ±0.5), (4.2 ±0.8) and (5.3 ±1.7) μg/L, and the LDH activities were (254 ±85), (275 ±75), (339 ±87) and (577 ±156) IU/L at T0-3 in the control group.The serum cTnI, CK-MB concentrations and LDH activities were higher at T2-3 than at T0 in the two groups ( P<0.05 or P<0.01) .Compared with the control group, the serum cTnI, CK-MB concentrations and LDH activ-ities at T2-3 were significantly decreased in the observation group (P<0.05 or P<0.01).The serum TNF-αlevels were (34 ±10), (38 ±11), (142 ±45) and (121 ±41) pg/mL, the serum IL-6 levels were (65 ±21), (70 ±24), (85 ± 23) and (102 ±33) pg/mL, and the serum IL-18 levels were (16 ±4), (18 ±6), (60 ±21) and (114 ±43) pg/mL at T0-3 in the observation group.The serum TNF-αlevels were (35 ±11), (43 ±12), (186 ±62) and (163 ±57) pg/mL, the serum IL-6 levels were (72 ±15), (82 ±23), (113 ±42) and (171 ±56) pg/mL, and the serum IL-18 levels were (17 ±5), (20 ±7), (78 ±23) and (153 ±51) pg/mL at T0-3 in the control group.The serum levels of TNF-α, IL-6 and IL-18 were higher at T2-3 than at T0 in the two groups (P<0.05 or P<0.01).Compared with the control group, the serum levels of TNF-α, IL-6 and IL-18 at T2-3 were significantly decreased in the observation group ( P<0.05 or P<0.01).Conclusion Ulinastatin preconditioning can alleviate cardiac injury in pediatric patients undergoing LRLT in a certain extent, whose mechanism may be related to inhibiting the excessive release of inflammatory factors.
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