高压氧治疗前后缺氧缺血性脑病新生儿心肌酶的变化

Changes of myocardial enzymes in newborns with hypoxic ischemic encephalopathy before and after hyperbaric oxygen treatment

目的:监测高压氧治疗前后新生儿缺氧缺血性脑病心肌酶谱的动态变化,以评价高压氧对新生儿缺氧缺血性脑病的应用价值。方法:①选择2001-12/2004-12解放军总医院第三○九临床部小儿内科足月缺氧缺血性脑病患儿76例。监护人同意参加。将患儿随机分为2组,每组38例,分别为高压氧治疗组和对照组。②两组全部给予常规治疗。高压氧治疗组在此基础上于入院24h内应用高压氧治疗,1次/d、共10次,高压氧舱为单人高压氧舱,以纯氧加压,压力为0.04～0.05MPa,加压10min,稳压40min,减压10min,稳压时舱内氧浓度72%～76%;两组患儿分别于治疗前及治疗后5和10d取股静脉血2mL,采用OLYMPUSAU600生化分析仪测定患儿5种心肌酶(谷草转氨酶、乳酸脱氢酶、α-羟丁酸脱氢酶、肌酸激酶、肌酸激酶同工酶)。③计量资料差异性测定采用t检验。结果:缺氧缺血性脑病患儿72例均进入结果分析。①高压氧治疗组治疗前缺氧缺血性脑病患儿5种心肌酶谷草转氨酶、乳酸脱氢酶、α-羟丁酸脱氢酶、肌酸激酶、肌酸激酶同工酶:与对照组治疗前接近(P>0.05)。②高压氧治疗组治疗后5和10d缺氧缺血性脑病患儿5种心肌酶水平明显低于对照组治疗后5和10d[高压氧治疗组治疗后5d:(2.50±0.58),(3.98±0.60),(4.80±0.58),(9.01±1.14),(1.71±0.27)μkat/L;高压氧治疗组治疗后10d(0.62±0.20),(2.80±0.41),(2.52±0.42),(2.60±0.38),(0.35±0.11)μkat/L;对照组治疗后5d:(4.76±0.54),(5.43±0.42),(7.38±0.64),(19.74±1.64),(3.43±0.54)μkat/L;对照组治疗后10d:(2.81±0.40),(4.27±0.70),(5.44±0.71),(13.11±1.08),(1.00±0.22)μkat/L,t=11.15～56.73,P<0.05)]。结论:①谷草转氨酶、肌酸激酶、肌酸激酶同工酶升高对心肌损害的诊断最有意义,而缺氧缺血性脑病的轻重与心肌损害的轻重相一致,亦与缺氧轻重相一致,故测定血清心肌酶对判断缺氧缺血性脑病病情非常重要。②高压氧0.04～0.05MPa可阻断缺氧所致脑组织的一系列病理过程,促使受损脑细胞尽快恢复。③常规治疗配合高压氧治疗可改善缺氧缺血性脑病患儿心肌酶。

AIM:To monitor the dynamic changes of myocardial zymogram in newborns with hypoxic ischemic encephalopathy before and after hyperbaric oxygen treatment, so as to assess the applicating value of hyperbaric oxygen in treating hypoxic ischemic encephalopathy. METHODS:①Seventy-six full-term newborns with hypoxic ischemic encephalopathy, who were born in the Department of Paediatrics, No.309 Clinical Division of General Hospital of Chinese PLA between December 2001 and December 2002, were involved in this study with the permission of their guardians. They were randomly divided into hyperbaric oxygen treatment group (n=38) and control group (n=38). ②All the patients received routine treatment, besides those in the hyperbaric oxygen treatment group were treated with hyperbaric oxygen within 24 hours after admission, once a day for 10 times. The hyperbaric oxygen chamber was a single one, compressed with pure oxygen, the pressure was 0.04 to 0.05 MPa, 10 minutes for compression, 40 minutes for pressure maintenance and 10 minutes for depression; The oxygen concentration in the chamber was 70 to 76% for oxygen maintenance. Before treatment and 5 and 10 days after treatment, 2 mL femoral venous blood was drawn in both groups, and OLYMPUS AU 600 biochemical analyzer was used to determine 5 kinds of myocardial enzymes (glutamic oxalacetic transaminase, lactate dehydrogenase, alpha-hydroxybutyrate dehydrogenase, creatine kinase, isoenzyme of creatine kinase). ③The difference of data was detected with the t test. RESULTS: All the 72 newborns with hypoxic ischemic encephalopathy were involved in the analysis of results.①The levels of glutamic oxalacetic transaminase, lactate dehydrogenase, alpha-hydroxybutyrate dehydrogenase, creatine kinase and isoenzyme of creatine kinase before treatment in the hyperbaric oxygen treatment group were close to those in the control group (P > 0.05).②The levels of the 5 enzymes in the newborns with hypoxic ischemic encephalopathy 5 and 10 days after treatment were obviously lower in the hyperbaric oxygen treatment group [5 days:(2.50±0.58), (3.98 ±0.60), (4.80±0.58), (9.01±1.14), (1.71±0.27) μkat/L; 10 days: (0.62±0.20), (2.80±0.41), (2.52±0.42), (2.60±0.38), (0.35±0.11) μkat/L] than in the control group [5 days: (4.76±0.54), (5.43±0.42), (7.38±0.64), (19.74±1.64), (3.43±0.54) μkat/L; 10 days: (2.81±0.40), (4.27±0.70), (5.44±0.71), (13.11±1.08), (1.00±0.22) μkat/L] (t=11.15 to 56.73, P < 0.05). CONCLUSION:①The increases of glutamic oxalacetic transaminase, creatine kinase and isoenzyme of creatine kinase are the most significant for the diagnosis of myocardial damage, and the severity of hypoxic ischemic encephalopathy is coincident with those of myocardial damage and hypoxia, so the determination of serum myocardial enzymes is very important for the judgement of hypoxic ischemic encephalopathy.②Hyperbaric oxygen of 0.04 to 0.05 MPa can block a series of pathological process of cerebral tissue caused by hypoxia, and accelerate the recovery of damaged cerebral cells as soon as possible.③ Routine treatment combined with hyperbaric oxygen treatment can ameliorate the myocardial enzymes in the newborns with hypoxic ischemic encephalopathy.