现代医药卫生
現代醫藥衛生
현대의약위생
MODERN MEDICINE HEALTH
2014年
17期
2589-2590
,共2页
心肌/病理学%磷酸肌酸%钠%缺血%缺氧%婴儿,早产
心肌/病理學%燐痠肌痠%鈉%缺血%缺氧%嬰兒,早產
심기/병이학%린산기산%납%결혈%결양%영인,조산
Myocardium/pathology%Phosphocreatine%Sodium%Ischemia%Anoxia%Infant,premature
目的:观察磷酸肌酸钠对早产儿缺氧缺血性心肌损伤的疗效。方法选择该院2009年7月至2011年11月收治的因窒息引起的心肌损伤早产儿104例,随机分为治疗组(56例)和对照组(48例),两组早产儿均给予常规治疗。治疗组在常规治疗的基础上给予磷酸肌酸钠0.5 g/d;对照组予维生素C 100 mg/kg,每天1次,1个疗程后(10 d)观察治疗前、后肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、心肌肌钙蛋白I(cTnI)的变化。结果治疗组早产儿治疗后CK、CK-MB和cTnI水平较对照组明显降低,差异均有统计学意义(P<0.05)。结论磷酸肌酸钠治疗早产儿缺氧缺血性心肌损伤有效。
目的:觀察燐痠肌痠鈉對早產兒缺氧缺血性心肌損傷的療效。方法選擇該院2009年7月至2011年11月收治的因窒息引起的心肌損傷早產兒104例,隨機分為治療組(56例)和對照組(48例),兩組早產兒均給予常規治療。治療組在常規治療的基礎上給予燐痠肌痠鈉0.5 g/d;對照組予維生素C 100 mg/kg,每天1次,1箇療程後(10 d)觀察治療前、後肌痠激酶(CK)、肌痠激酶同工酶(CK-MB)、心肌肌鈣蛋白I(cTnI)的變化。結果治療組早產兒治療後CK、CK-MB和cTnI水平較對照組明顯降低,差異均有統計學意義(P<0.05)。結論燐痠肌痠鈉治療早產兒缺氧缺血性心肌損傷有效。
목적:관찰린산기산납대조산인결양결혈성심기손상적료효。방법선택해원2009년7월지2011년11월수치적인질식인기적심기손상조산인104례,수궤분위치료조(56례)화대조조(48례),량조조산인균급여상규치료。치료조재상규치료적기출상급여린산기산납0.5 g/d;대조조여유생소C 100 mg/kg,매천1차,1개료정후(10 d)관찰치료전、후기산격매(CK)、기산격매동공매(CK-MB)、심기기개단백I(cTnI)적변화。결과치료조조산인치료후CK、CK-MB화cTnI수평교대조조명현강저,차이균유통계학의의(P<0.05)。결론린산기산납치료조산인결양결혈성심기손상유효。
Objective To observe the effect of creatine phosphate sodium on premature infants with hypoxic ischemic myocardial injury. Methods A total of 104 premature infants with hypoxic ischemic myocardial injury,who were in the hospital from June 2009 to November 2011,were randomized into treatment group(n=56)and control group(n=48). Based on the conven-tional therapy,the treatment group was added with creatine phosphate sodium,0.5 g daily;the control group was added with vita min C 100 mg/kg,once daily. After a course of treatment(10 d),the changes of creatine kinase(CK),CK-MB and cardiac tro-poninI(cTnI) in both groups were observed. Results After treatment,the levels of CK,CK-MB and cTnI of the premature infants in the treatment group reduced more obviously than those in the control group ,and the difference was statistically significant (P<0.05). Conclusion Creatine phosphate sodium is effective for the treatment of premature infants with hypoxic ischemic myocar-dial damage.