中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2012年
10期
1249-1251
,共3页
魏红芳%陈永学%李书河%杨晓彬%王新波%缪芸%吕航宇
魏紅芳%陳永學%李書河%楊曉彬%王新波%繆蕓%呂航宇
위홍방%진영학%리서하%양효빈%왕신파%무예%려항우
右美托咪啶%颅脑损伤%全身炎症反应综合征
右美託咪啶%顱腦損傷%全身炎癥反應綜閤徵
우미탁미정%로뇌손상%전신염증반응종합정
Dexmedetomidine%Craniocerebral trauma%Systemic inflammatory response syndrome
目的 探讨右美托咪定对急性颅脑损伤患者围术期炎性反应的影响.方法 颅脑损伤的患者70例,性别不限,年龄20 ~ 68岁,ASA分级Ⅰ~Ⅳ级,受伤24 h内行去骨瓣减压术,采用随机数字表法,将患者随机分为2组(n=35)∶对照组(C组)和右美托咪定组(D组).静脉注射芬太尼、异丙酚、顺阿曲库铵行麻醉诱导,术中均以瑞芬太尼、七氟醚、异丙酚维持麻醉,间断追加顺阿曲库铵.D组麻醉诱导前经10 min静脉输注右美托咪定1μg/kg,继以0.4 μg· kg-1·h-1的速率静脉输注2h.于麻醉诱导前、手术开始2h、术毕、术后24 h(T1 ~T4)时抽取静脉血样,测定血清神经元特异性烯醇化酶(NSE)、IL-6和TNF-α浓度.结果 与C组比较,D组血清NSE、TNF-α和IL-6浓度降低(P<0.05);与T1时比较,C组T2、T3时血清NSE、TNF-α和IL-6浓度升高,T4时血清TNF-α浓度降低,D组T2、T3时血清NSE和IL-6浓度升高,T4时降低,T3、T4时血清TNF-α浓度升高(P<0.05).结论 右美托咪定可通过抑制急性颅脑损伤患者围术期全身炎性反应,从而产生脑保护作用.
目的 探討右美託咪定對急性顱腦損傷患者圍術期炎性反應的影響.方法 顱腦損傷的患者70例,性彆不限,年齡20 ~ 68歲,ASA分級Ⅰ~Ⅳ級,受傷24 h內行去骨瓣減壓術,採用隨機數字錶法,將患者隨機分為2組(n=35)∶對照組(C組)和右美託咪定組(D組).靜脈註射芬太尼、異丙酚、順阿麯庫銨行痳醉誘導,術中均以瑞芬太尼、七氟醚、異丙酚維持痳醉,間斷追加順阿麯庫銨.D組痳醉誘導前經10 min靜脈輸註右美託咪定1μg/kg,繼以0.4 μg· kg-1·h-1的速率靜脈輸註2h.于痳醉誘導前、手術開始2h、術畢、術後24 h(T1 ~T4)時抽取靜脈血樣,測定血清神經元特異性烯醇化酶(NSE)、IL-6和TNF-α濃度.結果 與C組比較,D組血清NSE、TNF-α和IL-6濃度降低(P<0.05);與T1時比較,C組T2、T3時血清NSE、TNF-α和IL-6濃度升高,T4時血清TNF-α濃度降低,D組T2、T3時血清NSE和IL-6濃度升高,T4時降低,T3、T4時血清TNF-α濃度升高(P<0.05).結論 右美託咪定可通過抑製急性顱腦損傷患者圍術期全身炎性反應,從而產生腦保護作用.
목적 탐토우미탁미정대급성로뇌손상환자위술기염성반응적영향.방법 로뇌손상적환자70례,성별불한,년령20 ~ 68세,ASA분급Ⅰ~Ⅳ급,수상24 h내행거골판감압술,채용수궤수자표법,장환자수궤분위2조(n=35)∶대조조(C조)화우미탁미정조(D조).정맥주사분태니、이병분、순아곡고안행마취유도,술중균이서분태니、칠불미、이병분유지마취,간단추가순아곡고안.D조마취유도전경10 min정맥수주우미탁미정1μg/kg,계이0.4 μg· kg-1·h-1적속솔정맥수주2h.우마취유도전、수술개시2h、술필、술후24 h(T1 ~T4)시추취정맥혈양,측정혈청신경원특이성희순화매(NSE)、IL-6화TNF-α농도.결과 여C조비교,D조혈청NSE、TNF-α화IL-6농도강저(P<0.05);여T1시비교,C조T2、T3시혈청NSE、TNF-α화IL-6농도승고,T4시혈청TNF-α농도강저,D조T2、T3시혈청NSE화IL-6농도승고,T4시강저,T3、T4시혈청TNF-α농도승고(P<0.05).결론 우미탁미정가통과억제급성로뇌손상환자위술기전신염성반응,종이산생뇌보호작용.
Objective To investigate the effect of dexmedetomidine on inflammatory response during the perioperative period in patients with acute craniocerebral trauma.Methods Seventy ASA Ⅰ-Ⅳ patients of both sexes,aged 20-68 yr,with craniocerebral trauma,who required decompressive craniectomy within the next 24 h,were randomly divided into 2 groups (n =35 each) ∶ control group (group C) and dexmedetomidine group (group D).Anesthesia was induced with fentanyl,propofol and cisatracurium and maintained with remifentanil,sevoflurane and propofol and intermittent iv boluses of cisatracurium.In group D,dexmedetomidine 1 μg/kg was infused over 10 min,followed by infusion at 0.4 μg· kg-1 · h-1 for 2 h.Venous blood samples were taken before induction of anesthesia (baseline),2 h after the beginning of operation,at the end of operation and at 24 h after operation (T1-T4) to determine the concentrations of serum neurone specific enolase (NSE),interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α).Results Compared with group C,the concentrations of serum NSE,IL-6 and TNF-α were significantly decreased in group D (P < 0.05).The concentrations of serum NSE,IL-6 and TNF-αwere significantly higher at T2 and T3,and the concentration of serum TNF-α was significantly lower at T4 than at T1 in group C (P < 0.05).The concentrations of serum NSE and IL-6 were significantly higher at T2 and T3 and lower at T4 and the concentration of serum TNF-α was significantly higher at T3 and T4 than at T1 in group D (P <0.05).Conclusion Dexmedetomidine protects the brain against acute craniocerebral trauma by inhibiting systemic inflammatory response during the perioperative period.