中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2009年
9期
846-848
,共3页
安替比林%缺氧缺血%脑%婴儿%新生
安替比林%缺氧缺血%腦%嬰兒%新生
안체비림%결양결혈%뇌%영인%신생
Antipyrine%Hypoxia-ischemia,Brain%Infant,newborn
目的 探讨依达拉奉对新生猪缺氧缺血性脑损伤的影响.方法 出生3～7 d的雄性猪,体重2.0～3.0 kg,采用窒息性心搏骤停后心肺复苏的方法制备缺氧缺血性脑损伤模型.取自主循环恢复(ROSC)的新生猪20头随机分为2组(n=10):脑缺氧缺血组(HI组)和依达拉奉组(E组),另取10头作为假手术组(S组).ROSC后30 min,E组静脉注射依达拉奉3 mg/kg,随后静脉输注,速率为1.5 mg·kg~(-1)·h~(-1),输注时间5.5 h,HI组以溶剂替代依达拉奉.于ROSC后48、72和96 h时行神经功能损伤评分,于ROSC后96 h时测定脑组织8-羟基(脱氧)鸟苷(8-OHdG/OHG)表达水平,光镜下观察脑组织病理学结果,并计算存活神经元密度.结果 与S组比较,HI组和E组脑组织存活神经元密度降低,8-OHdG/OHG表达水平升高,神经功能损伤评分升高(P<0.01);与HI组比较,E组脑组织存活神经元密度升高,8-OHdG/OHG表达水平降低,E组ROSC后48 h时神经功能损伤评分降低(P<0.05);E组脑组织病理学损伤较HI组减轻.结论 依达拉奉可减轻新生猪缺氧缺血性脑损伤,其机制可能与减轻DNA/RNA氧化损伤有关.
目的 探討依達拉奉對新生豬缺氧缺血性腦損傷的影響.方法 齣生3～7 d的雄性豬,體重2.0～3.0 kg,採用窒息性心搏驟停後心肺複囌的方法製備缺氧缺血性腦損傷模型.取自主循環恢複(ROSC)的新生豬20頭隨機分為2組(n=10):腦缺氧缺血組(HI組)和依達拉奉組(E組),另取10頭作為假手術組(S組).ROSC後30 min,E組靜脈註射依達拉奉3 mg/kg,隨後靜脈輸註,速率為1.5 mg·kg~(-1)·h~(-1),輸註時間5.5 h,HI組以溶劑替代依達拉奉.于ROSC後48、72和96 h時行神經功能損傷評分,于ROSC後96 h時測定腦組織8-羥基(脫氧)鳥苷(8-OHdG/OHG)錶達水平,光鏡下觀察腦組織病理學結果,併計算存活神經元密度.結果 與S組比較,HI組和E組腦組織存活神經元密度降低,8-OHdG/OHG錶達水平升高,神經功能損傷評分升高(P<0.01);與HI組比較,E組腦組織存活神經元密度升高,8-OHdG/OHG錶達水平降低,E組ROSC後48 h時神經功能損傷評分降低(P<0.05);E組腦組織病理學損傷較HI組減輕.結論 依達拉奉可減輕新生豬缺氧缺血性腦損傷,其機製可能與減輕DNA/RNA氧化損傷有關.
목적 탐토의체랍봉대신생저결양결혈성뇌손상적영향.방법 출생3～7 d적웅성저,체중2.0～3.0 kg,채용질식성심박취정후심폐복소적방법제비결양결혈성뇌손상모형.취자주순배회복(ROSC)적신생저20두수궤분위2조(n=10):뇌결양결혈조(HI조)화의체랍봉조(E조),령취10두작위가수술조(S조).ROSC후30 min,E조정맥주사의체랍봉3 mg/kg,수후정맥수주,속솔위1.5 mg·kg~(-1)·h~(-1),수주시간5.5 h,HI조이용제체대의체랍봉.우ROSC후48、72화96 h시행신경공능손상평분,우ROSC후96 h시측정뇌조직8-간기(탈양)조감(8-OHdG/OHG)표체수평,광경하관찰뇌조직병이학결과,병계산존활신경원밀도.결과 여S조비교,HI조화E조뇌조직존활신경원밀도강저,8-OHdG/OHG표체수평승고,신경공능손상평분승고(P<0.01);여HI조비교,E조뇌조직존활신경원밀도승고,8-OHdG/OHG표체수평강저,E조ROSC후48 h시신경공능손상평분강저(P<0.05);E조뇌조직병이학손상교HI조감경.결론 의체랍봉가감경신생저결양결혈성뇌손상,기궤제가능여감경DNA/RNA양화손상유관.
Objective To investigate the effects of endaravane on hypoxia-ischemia (HI)-induced brain injury in neonatal piglets. Methods Male piglets 3-7 days old weighing 2.0-3.0 kg were used in this study. Group Ⅰ 10 piglets were randomly collected as sham operation without HI. Twenty piglets with HI were randomly divided into 2 groups (n = 10 each) : group Ⅱ HI and group Ⅲ HI + endaravone. The animals were anesthetized with intraperitoneal pentobarbital sodium 50 mg/kg, tracheostomized and mechanically ventilated with 30% O_2. Right femoral artery and vein were cannulated. MAP, HR, PET CO_2, blood gases and glucose and rectal temperature were monitored. After 15 min stabilization cardiac arrest was induced by inhalation of hypoxic air (O_2 10%) for 40 min followed by inhalation of 21% O_2 for 5 min. The tracheal tube was then occluded for 7 min. Cardio-pulmonary resuscitation (CPR) was then started until recovery of spontaneous circulation (ROSC). CPR > 3 min was considered a failure. A bolus of endaravone 3 mg/kg was given iv over an hour at 30 min after CPR,followed by continuous infusion at 1.5 mg·kg~(-1)·h~(-1) for 5.5 h in group Ⅲ , while in group Ⅱ vehicle was given instead of endaravone. The neurological function of the animals was evaluated at 48, 72 and 96 h after ROSC and scored (0-154, 0 = normal, 154 = severest dysfunction). The animals were killed at 96 h after ROSC. The brains were removed for microscopic examination of striatum and cortex and determination of 8-hydroxy-2'-deoxyguanine (8-OHdG/OHG) expression in putamen by immuno-histochemistry. Results The neurological function scores were significantly higher at 48 h after ROSC and the number of viable neurons in striatum and sensory cortex were significantly lower and the expression of 8-OHdG/OHG in putamen was significantly higher in group Ⅱ than in group Ⅲ . Conclusion The antioxidant endaravone given after CPR can attenuate Hl-induced brain injury by inhibiting oxidative damage to DNA and RNA.
