国际麻醉学与复苏杂志
國際痳醉學與複囌雜誌
국제마취학여복소잡지
INTERNATIONAL JOURNAL OF ANESTHESIOLOGY AND RESUSCITATION
2014年
6期
502-505
,共4页
吴周晏%吉杰梅%谷万杰%刘文志%刘敬臣
吳週晏%吉傑梅%穀萬傑%劉文誌%劉敬臣
오주안%길걸매%곡만걸%류문지%류경신
右美托咪定%脂多糖%急性肺损伤
右美託咪定%脂多糖%急性肺損傷
우미탁미정%지다당%급성폐손상
Dexmedetomidine%Lipopolysaccharide%Acute lung injury
目的 探讨右美托咪定(dexmedetomidine,Dex)预先给药对脂多糖(lipopolysaccharide,LPS)诱导大鼠急性肺损伤(acute lung injury,ALI)的保护作用. 方法 气管滴注LPS 5 mg/kg,建立大鼠ALI模型.30只雄性SD大鼠,采用随机数字表法分为3组,每组10只:空白对照组(C组,输注生理盐水)、LPS对照组(L组,腹腔注射生理盐水30 min后气管滴注LPS)、Dex预先给药组(D组,腹腔注射Dex 50 μg/kg 30 min后气管滴注LPS).注射LPS后6h处死动物,行动脉血气分析、检测肺组织髓过氧化物酶(myeloperoxidase,MPO)活性、肺组织湿/干重比(wet/dry ratio,W/D)、肿瘤坏死因子-α(tumor necrosis factor-alpha,TNF-α)和白介素-6(interleukin-6,IL-6),观察肺组织病理学的改变. 结果 D组与L组比较,MPO活性水平分别为(0.70±0.06)和(1.01 ±0.05)(P＜0.01)、肺组织W/D值分别为(4.44±0.08)和(4.76±0.10)(P＜0.01)、动脉血氧分压(oxygen partialpressure of the artery,Pa02)值分别为(94.0±2.6) mmHg(1 mmHg=0.133 kPa)和(78.0±4.7) mmHg(P＜0.05)、血清TNF-α值分别为(39±9) ng/L和(92±14) ng/L(P＜0.05)、IL-6值分别为(72±16) ng/L和(95±16)ng/L(P＜0.05),且D组肺损伤的病理的严重程度比L组轻. 结论 Dex预先给药对LPS诱导大鼠AH有一定的保护作用,与抑制中性粒细胞在肺内聚集、激活和TNF-α、IL-6等炎性因子的释放有关.
目的 探討右美託咪定(dexmedetomidine,Dex)預先給藥對脂多糖(lipopolysaccharide,LPS)誘導大鼠急性肺損傷(acute lung injury,ALI)的保護作用. 方法 氣管滴註LPS 5 mg/kg,建立大鼠ALI模型.30隻雄性SD大鼠,採用隨機數字錶法分為3組,每組10隻:空白對照組(C組,輸註生理鹽水)、LPS對照組(L組,腹腔註射生理鹽水30 min後氣管滴註LPS)、Dex預先給藥組(D組,腹腔註射Dex 50 μg/kg 30 min後氣管滴註LPS).註射LPS後6h處死動物,行動脈血氣分析、檢測肺組織髓過氧化物酶(myeloperoxidase,MPO)活性、肺組織濕/榦重比(wet/dry ratio,W/D)、腫瘤壞死因子-α(tumor necrosis factor-alpha,TNF-α)和白介素-6(interleukin-6,IL-6),觀察肺組織病理學的改變. 結果 D組與L組比較,MPO活性水平分彆為(0.70±0.06)和(1.01 ±0.05)(P＜0.01)、肺組織W/D值分彆為(4.44±0.08)和(4.76±0.10)(P＜0.01)、動脈血氧分壓(oxygen partialpressure of the artery,Pa02)值分彆為(94.0±2.6) mmHg(1 mmHg=0.133 kPa)和(78.0±4.7) mmHg(P＜0.05)、血清TNF-α值分彆為(39±9) ng/L和(92±14) ng/L(P＜0.05)、IL-6值分彆為(72±16) ng/L和(95±16)ng/L(P＜0.05),且D組肺損傷的病理的嚴重程度比L組輕. 結論 Dex預先給藥對LPS誘導大鼠AH有一定的保護作用,與抑製中性粒細胞在肺內聚集、激活和TNF-α、IL-6等炎性因子的釋放有關.
목적 탐토우미탁미정(dexmedetomidine,Dex)예선급약대지다당(lipopolysaccharide,LPS)유도대서급성폐손상(acute lung injury,ALI)적보호작용. 방법 기관적주LPS 5 mg/kg,건립대서ALI모형.30지웅성SD대서,채용수궤수자표법분위3조,매조10지:공백대조조(C조,수주생리염수)、LPS대조조(L조,복강주사생리염수30 min후기관적주LPS)、Dex예선급약조(D조,복강주사Dex 50 μg/kg 30 min후기관적주LPS).주사LPS후6h처사동물,행동맥혈기분석、검측폐조직수과양화물매(myeloperoxidase,MPO)활성、폐조직습/간중비(wet/dry ratio,W/D)、종류배사인자-α(tumor necrosis factor-alpha,TNF-α)화백개소-6(interleukin-6,IL-6),관찰폐조직병이학적개변. 결과 D조여L조비교,MPO활성수평분별위(0.70±0.06)화(1.01 ±0.05)(P＜0.01)、폐조직W/D치분별위(4.44±0.08)화(4.76±0.10)(P＜0.01)、동맥혈양분압(oxygen partialpressure of the artery,Pa02)치분별위(94.0±2.6) mmHg(1 mmHg=0.133 kPa)화(78.0±4.7) mmHg(P＜0.05)、혈청TNF-α치분별위(39±9) ng/L화(92±14) ng/L(P＜0.05)、IL-6치분별위(72±16) ng/L화(95±16)ng/L(P＜0.05),차D조폐손상적병리적엄중정도비L조경. 결론 Dex예선급약대LPS유도대서AH유일정적보호작용,여억제중성립세포재폐내취집、격활화TNF-α、IL-6등염성인자적석방유관.
Objective To investigate the protective effect of dexmedetomidine(Dex) pretreatment on acute lung injury(ALI) induced by lipopolysaccharide (LPS) in rats.Methods A total of 30 male Sprague-Dawley rats were randomly divided into three groups(n=10):control gronp (group C),the LPS group (group L) and the Dex pretreatment group (group D).The rats in the LPS group were intratracheally administered with LPS (5 mg/kg) to duplicate an acute lung injury model.In the group D,the rats were given 50 μg/kg of Dex intraperitoneally 30 min before LPS application.Six hours after LPS administration,arterial blood was drawn for interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) measurement,and the pulmonary tissues were harvested for pathological evaluation,wet/dry (W/D) ratio measurement,biochemical analysis of myeloperoxidase (MPO).Results The Dex pretreatment group compared with LPS group,the levels of wet/dry weight ratio were (4.44±0.08) and (4.76±0.10) respectively (P＜0.O1),the levels of MPO activities were (0.70±0.06) and (1.01±0.05) respectively (P＜0.01).The value of the oxygen partial pressure in the arteries were (94.0±2.6) mmHg (1 mmHg=0.133 kPa) and (78.0±4.7) mmHg respectively (P＜0.05).The levels of TNF-α were (39±9) ng/L and (92±14) ng/L respectively(P＜0.05).The levels of IL-6 were (72±16) ng/L and (95±16) ng/L respectively(P＜0.05).The pulmonary tissue damage in histopathology in LPS group was more severe than in Dex pretreatment group.Conclusions Dex pretreatment can protect acute lung injury induced by LPS through inhibition of activation of neutrophil in lung tissue and expression of TNF-α and IL-6.
