中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
5期
608-611
,共4页
张玮玮%郭永清%余淑珍%荆建敏%卫建峰
張瑋瑋%郭永清%餘淑珍%荊建敏%衛建峰
장위위%곽영청%여숙진%형건민%위건봉
自由基清除剂%心肌再灌注损伤%呼吸窘迫综合征,成人
自由基清除劑%心肌再灌註損傷%呼吸窘迫綜閤徵,成人
자유기청제제%심기재관주손상%호흡군박종합정,성인
Free radical scavengers%Myocardial reperfusion injury%Respiratory distress syndrome,adult
目的 探讨依达拉奉对大鼠心肌缺血再灌注诱发肺损伤的影响.方法 健康清洁级雄性Wistar大鼠24只,体重250~300 g,随机分为4组(n=6):假手术组(S组)、心肌缺血再灌注组(IR组)和不同剂量依达拉奉组(E1组和E2组).IR组、E1组和E2组采用结扎冠状动脉左前降支(LAD)45 min,再灌注3 h的方法制备心肌缺血再灌注模型.S组仅LAD下穿线不结扎;IR组阻断LAD45 min后再灌注3 h;E1组和E2组分别于再灌注前1 min经右股静脉注射依达拉奉3或10 mg/kg.于再灌注3 h时放血处死大鼠,取肺组织、支气管肺泡灌洗液和动脉血样,测定血清肌酸激酶同工酶(CK-MB)活性,计算肺通透性指数(PPI),采用Western blot法检测肺组织β-防御素-2(BD-2)和TNF-α蛋白的表达,PCR法测定肺组织BD-2 mRNA表达.结果 与S组比较,IR组、E1组和E2组血清CK-MB活性和PPI升高,肺组织BD-2 mRNA、BD-2和TNF-α蛋白表达上调(P<0.01).与IR组比较,E1组和E2组血清CK-MB活性和PPI降低,肺组织BD-2 mRNA、BD-2和TNF-α蛋白表达下调(P<0.01).与E1组比较,E2组血清CK-MB活性和PPI降低,肺组织BD-2 mRNA、BD-2和TNF-α蛋白表达下调(P<0.01).结论 依达拉奉可减轻大鼠心肌缺血再灌注诱发的肺损伤,其机制不仅与清除氧自由基有关,还与抑制肺组织炎性反应有关.
目的 探討依達拉奉對大鼠心肌缺血再灌註誘髮肺損傷的影響.方法 健康清潔級雄性Wistar大鼠24隻,體重250~300 g,隨機分為4組(n=6):假手術組(S組)、心肌缺血再灌註組(IR組)和不同劑量依達拉奉組(E1組和E2組).IR組、E1組和E2組採用結扎冠狀動脈左前降支(LAD)45 min,再灌註3 h的方法製備心肌缺血再灌註模型.S組僅LAD下穿線不結扎;IR組阻斷LAD45 min後再灌註3 h;E1組和E2組分彆于再灌註前1 min經右股靜脈註射依達拉奉3或10 mg/kg.于再灌註3 h時放血處死大鼠,取肺組織、支氣管肺泡灌洗液和動脈血樣,測定血清肌痠激酶同工酶(CK-MB)活性,計算肺通透性指數(PPI),採用Western blot法檢測肺組織β-防禦素-2(BD-2)和TNF-α蛋白的錶達,PCR法測定肺組織BD-2 mRNA錶達.結果 與S組比較,IR組、E1組和E2組血清CK-MB活性和PPI升高,肺組織BD-2 mRNA、BD-2和TNF-α蛋白錶達上調(P<0.01).與IR組比較,E1組和E2組血清CK-MB活性和PPI降低,肺組織BD-2 mRNA、BD-2和TNF-α蛋白錶達下調(P<0.01).與E1組比較,E2組血清CK-MB活性和PPI降低,肺組織BD-2 mRNA、BD-2和TNF-α蛋白錶達下調(P<0.01).結論 依達拉奉可減輕大鼠心肌缺血再灌註誘髮的肺損傷,其機製不僅與清除氧自由基有關,還與抑製肺組織炎性反應有關.
목적 탐토의체랍봉대대서심기결혈재관주유발폐손상적영향.방법 건강청길급웅성Wistar대서24지,체중250~300 g,수궤분위4조(n=6):가수술조(S조)、심기결혈재관주조(IR조)화불동제량의체랍봉조(E1조화E2조).IR조、E1조화E2조채용결찰관상동맥좌전강지(LAD)45 min,재관주3 h적방법제비심기결혈재관주모형.S조부LAD하천선불결찰;IR조조단LAD45 min후재관주3 h;E1조화E2조분별우재관주전1 min경우고정맥주사의체랍봉3혹10 mg/kg.우재관주3 h시방혈처사대서,취폐조직、지기관폐포관세액화동맥혈양,측정혈청기산격매동공매(CK-MB)활성,계산폐통투성지수(PPI),채용Western blot법검측폐조직β-방어소-2(BD-2)화TNF-α단백적표체,PCR법측정폐조직BD-2 mRNA표체.결과 여S조비교,IR조、E1조화E2조혈청CK-MB활성화PPI승고,폐조직BD-2 mRNA、BD-2화TNF-α단백표체상조(P<0.01).여IR조비교,E1조화E2조혈청CK-MB활성화PPI강저,폐조직BD-2 mRNA、BD-2화TNF-α단백표체하조(P<0.01).여E1조비교,E2조혈청CK-MB활성화PPI강저,폐조직BD-2 mRNA、BD-2화TNF-α단백표체하조(P<0.01).결론 의체랍봉가감경대서심기결혈재관주유발적폐손상,기궤제불부여청제양자유기유관,환여억제폐조직염성반응유관.
Objective To investigate the effects of edaranvone on lung injury induced by myocardial ischemia-reperfusion (I/R) in rats. Methods Twenty-four male Wistar rats weighing 250-300 g were randomly assigned to one of 4 groups ( n = 6 each): group Ⅰ sham operation (group S); group Ⅱ myocardial I/R and group Ⅲ and Ⅳ different doses of edaravone ( group E1, E2 ). The animals were anesthetized, intubated and mechanically ventilated. In group Ⅱ-Ⅳ myocardial I/R was induced by occlusion of left anterior descending coronary artery for 45 min followed by 3 h reperfusion. In group Ⅲ and Ⅳ edavarone 3 and 10 mg/kg was administered via right femoral vein at 1 min before reperfusion respectively. The animals were sacrificed by exsanguination at the end of 3 h reperfusion. Blood was collected for determination of serum CK-MB activity and total protein content. The left lung was lavaged and the broncho-alveolar lavage fluid (BALF) was colleted for determination of protein content. Pulmonary permeability index (PPI) was calculated. The lung tissue was obtained for determination of BD-2 mRNA and protein and TNF-α expression. Results The serum CK-MB activity, PPI,BD-2 mRNA and protein and TNF-α expression were significantly higher in group I/R, E1 and E2 than in group S,but significantly lower in group E1 and E2 than in group I/R and in group E2 than in group E1. Conclusion Edaravone can reduce myocardial I/R-induced lung injury by scavenging oxygen free radicals and inhibiting inflammatory response of lung tissues in rats.