中国医药
中國醫藥
중국의약
CHINA MEDICINE
2013年
2期
162-164
,共3页
张奕威%戴何兴%陆东健%刘光晃%苏月南
張奕威%戴何興%陸東健%劉光晃%囌月南
장혁위%대하흥%륙동건%류광황%소월남
呼吸窘迫综合征,成人%急性肺损伤%靶器官保护%肺保护
呼吸窘迫綜閤徵,成人%急性肺損傷%靶器官保護%肺保護
호흡군박종합정,성인%급성폐손상%파기관보호%폐보호
Respiratory distress syndrome,adult%Acute lung injury%Target organ protection%Lung protection
目的 探讨靶器官保护策略对急性肺损伤的防护作用.方法 将急性肺损伤患者85例完全随机分为对照组(42例)和研究组(43例).2组给予常规治疗,研究组为保护炎症靶器官(肠道、肺脏)加用①生大黄30 g,水煎成200 ml溶液(水煎15 min),分2次/d口服或管饲；②静脉滴注盐酸氨溴索60 mg,2次/d；③静脉注射乌司他丁40万U,1次/8 h,疗程7d.监测患者治疗前后呼吸频率、PaO2、氧合指数、血清中肿瘤坏死因子-α(TNF-α)、白细胞介素6(IL-6)、IL-8水平、7d后全身炎症反应综合征(SIRS)评分及预后情况.结果 2组治疗前各项监测指标差异无统计学意义,治疗后研究组患者呼吸频率、PaO2、氧合指数、SIRS评分明显优于对照组(P＜0.05)；研究组TNF-α、IL-6、IL-8于治疗第3天明显下降,改善均优于对照组(P＜0.05).研究组7d后SIRS评分低于对照组,但差异无统计学意义[(1.7±1.3)分比(2.6±1.3)分,P＞0.05]；ARDS发生率低于对照组[29.2％(12/43)比59.5％ (25/42),P＜0.05]；病死率虽低于对照组,但差异无统计学意义[18.6％ (8/43)比25.6％ (11/42),P＞0.05].结论 注重炎症靶器官保护可抑制炎症介质产生、释放和体内炎症反应的放大,提供肺保护作用.
目的 探討靶器官保護策略對急性肺損傷的防護作用.方法 將急性肺損傷患者85例完全隨機分為對照組(42例)和研究組(43例).2組給予常規治療,研究組為保護炎癥靶器官(腸道、肺髒)加用①生大黃30 g,水煎成200 ml溶液(水煎15 min),分2次/d口服或管飼；②靜脈滴註鹽痠氨溴索60 mg,2次/d；③靜脈註射烏司他丁40萬U,1次/8 h,療程7d.鑑測患者治療前後呼吸頻率、PaO2、氧閤指數、血清中腫瘤壞死因子-α(TNF-α)、白細胞介素6(IL-6)、IL-8水平、7d後全身炎癥反應綜閤徵(SIRS)評分及預後情況.結果 2組治療前各項鑑測指標差異無統計學意義,治療後研究組患者呼吸頻率、PaO2、氧閤指數、SIRS評分明顯優于對照組(P＜0.05)；研究組TNF-α、IL-6、IL-8于治療第3天明顯下降,改善均優于對照組(P＜0.05).研究組7d後SIRS評分低于對照組,但差異無統計學意義[(1.7±1.3)分比(2.6±1.3)分,P＞0.05]；ARDS髮生率低于對照組[29.2％(12/43)比59.5％ (25/42),P＜0.05]；病死率雖低于對照組,但差異無統計學意義[18.6％ (8/43)比25.6％ (11/42),P＞0.05].結論 註重炎癥靶器官保護可抑製炎癥介質產生、釋放和體內炎癥反應的放大,提供肺保護作用.
목적 탐토파기관보호책략대급성폐손상적방호작용.방법 장급성폐손상환자85례완전수궤분위대조조(42례)화연구조(43례).2조급여상규치료,연구조위보호염증파기관(장도、폐장)가용①생대황30 g,수전성200 ml용액(수전15 min),분2차/d구복혹관사；②정맥적주염산안추색60 mg,2차/d；③정맥주사오사타정40만U,1차/8 h,료정7d.감측환자치료전후호흡빈솔、PaO2、양합지수、혈청중종류배사인자-α(TNF-α)、백세포개소6(IL-6)、IL-8수평、7d후전신염증반응종합정(SIRS)평분급예후정황.결과 2조치료전각항감측지표차이무통계학의의,치료후연구조환자호흡빈솔、PaO2、양합지수、SIRS평분명현우우대조조(P＜0.05)；연구조TNF-α、IL-6、IL-8우치료제3천명현하강,개선균우우대조조(P＜0.05).연구조7d후SIRS평분저우대조조,단차이무통계학의의[(1.7±1.3)분비(2.6±1.3)분,P＞0.05]；ARDS발생솔저우대조조[29.2％(12/43)비59.5％ (25/42),P＜0.05]；병사솔수저우대조조,단차이무통계학의의[18.6％ (8/43)비25.6％ (11/42),P＞0.05].결론 주중염증파기관보호가억제염증개질산생、석방화체내염증반응적방대,제공폐보호작용.
Objective To investigate the preventive and protective effect of target organ protection strategy on acute lung injury.Methods Eighty-five acute lung injury patients were randomly divided into two groups; control group(n =42) was treated commonly and research group (n =43) was treated with target organ protected treatment protocols besides the conventional therapy for 7 days.Respiratory rate,oxygenation index,systemic inflammatory response syndrome (SIRS) scores,tumor necrosis factor α (TNF-α),interleukin 6 (IL-6) and IL-8 were analyzed.Results The differences between two groups were not statistically significant before treatment (P ＞ 0.05).The contrast of respiratory rate,oxygenation index,PaO2 and SIRS scores between two groups were statistically significant (P ＜ 0.05) ; the contrast of TNF-α,IL-6,IL-8 between two groups were statistically significant (P ＜0.05) after treatment.The incidence of acute respiratory distress syndrome (ARDS) of experimental group reduced relatively [29.2％ (12/43) vs 59.5％ (25/42),P ＜ 0.05] ; the mortality between two groups was not statistically significant [18.6％ (8/43) vs 25.6％ (11/42),P ＞ 0.05].Conclusions Emphasizing protecting inflammatory target organ can restrain inflammatory mediators creation and releasing,interrupt the amplification of inflammatory response and protect the pulmonary function.
