中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2013年
9期
1138-1141
,共4页
曹惠鹃%裴凌%于冬梅%张瑜%周锦
曹惠鵑%裴凌%于鼕梅%張瑜%週錦
조혜견%배릉%우동매%장유%주금
胆碱能拮抗剂%呼吸窘迫综合征,成人%内毒素血症%血管生成素1%受体蛋白质酪氨酸激酶类
膽堿能拮抗劑%呼吸窘迫綜閤徵,成人%內毒素血癥%血管生成素1%受體蛋白質酪氨痠激酶類
담감능길항제%호흡군박종합정,성인%내독소혈증%혈관생성소1%수체단백질락안산격매류
Cholinergic antagonist%Respiratory distress syndrome,adult%Endotoxemia%Angiopoietin-1%Receptor,protein-tyrosine kinases
目的 评价盐酸戊乙奎醚对大鼠内毒素性急性肺损伤时血管生成素-1(Ang-1)和酪氨酸激酶受体-2(Tie-2)水平的影响.方法 成年雄性SD大鼠40只,4～6月龄,体重180 ～ 220 g,采用随机数字表法,将其分为4组(n=10):对照组(C组)、肺损伤组(ALI组)、盐酸戊乙奎醚低剂量组(L-PHC组)和盐酸戊乙奎醚高剂量组(H-PHC组).ALI组尾静脉注射脂多糖(LPS)5.0 mg/kg,L-PHC组和H-PHC组于静脉注射LPS后1和24 h时分别尾静脉注射盐酸戊乙奎醚0.6、2.0 mg/kg.于首次注射盐酸戊乙奎醚后48 h时,处死大鼠,测定肺组织含水量、支气管肺泡灌洗液(BALF)蛋白浓度和肺组织Ang-1、Tie-2及磷酸化Tie-2的表达(Western blot法),光镜下观察肺组织病理学结果,透射电镜下观察肺泡上皮屏障结构.结果 与C组比较,ALI组、L-PHC组和H-PHC组肺组织含水量、BALF蛋白浓度升高,肺组织Ang-1和磷酸化Tie-2表达下调(P＜0.05)；与ALI组比较,H-PHC组肺组织含水量、BALF蛋白浓度降低,肺组织Ang-1和磷酸化Tie-2表达上调(P＜0.05),L-PHC组上述指标差异无统计学意义(P＞0.05).H-PHC组肺组织损伤较ALI组减轻.结论 盐酸戊乙奎醚可改善肺血管环通透性,减轻肺泡上皮屏障损伤,从而减轻大鼠内毒素性急性肺损伤,且该作用与剂量有关,其机制与上调Ang-1表达和增强Tie-2活性有关.
目的 評價鹽痠戊乙奎醚對大鼠內毒素性急性肺損傷時血管生成素-1(Ang-1)和酪氨痠激酶受體-2(Tie-2)水平的影響.方法 成年雄性SD大鼠40隻,4～6月齡,體重180 ～ 220 g,採用隨機數字錶法,將其分為4組(n=10):對照組(C組)、肺損傷組(ALI組)、鹽痠戊乙奎醚低劑量組(L-PHC組)和鹽痠戊乙奎醚高劑量組(H-PHC組).ALI組尾靜脈註射脂多糖(LPS)5.0 mg/kg,L-PHC組和H-PHC組于靜脈註射LPS後1和24 h時分彆尾靜脈註射鹽痠戊乙奎醚0.6、2.0 mg/kg.于首次註射鹽痠戊乙奎醚後48 h時,處死大鼠,測定肺組織含水量、支氣管肺泡灌洗液(BALF)蛋白濃度和肺組織Ang-1、Tie-2及燐痠化Tie-2的錶達(Western blot法),光鏡下觀察肺組織病理學結果,透射電鏡下觀察肺泡上皮屏障結構.結果 與C組比較,ALI組、L-PHC組和H-PHC組肺組織含水量、BALF蛋白濃度升高,肺組織Ang-1和燐痠化Tie-2錶達下調(P＜0.05)；與ALI組比較,H-PHC組肺組織含水量、BALF蛋白濃度降低,肺組織Ang-1和燐痠化Tie-2錶達上調(P＜0.05),L-PHC組上述指標差異無統計學意義(P＞0.05).H-PHC組肺組織損傷較ALI組減輕.結論 鹽痠戊乙奎醚可改善肺血管環通透性,減輕肺泡上皮屏障損傷,從而減輕大鼠內毒素性急性肺損傷,且該作用與劑量有關,其機製與上調Ang-1錶達和增彊Tie-2活性有關.
목적 평개염산무을규미대대서내독소성급성폐손상시혈관생성소-1(Ang-1)화락안산격매수체-2(Tie-2)수평적영향.방법 성년웅성SD대서40지,4～6월령,체중180 ～ 220 g,채용수궤수자표법,장기분위4조(n=10):대조조(C조)、폐손상조(ALI조)、염산무을규미저제량조(L-PHC조)화염산무을규미고제량조(H-PHC조).ALI조미정맥주사지다당(LPS)5.0 mg/kg,L-PHC조화H-PHC조우정맥주사LPS후1화24 h시분별미정맥주사염산무을규미0.6、2.0 mg/kg.우수차주사염산무을규미후48 h시,처사대서,측정폐조직함수량、지기관폐포관세액(BALF)단백농도화폐조직Ang-1、Tie-2급린산화Tie-2적표체(Western blot법),광경하관찰폐조직병이학결과,투사전경하관찰폐포상피병장결구.결과 여C조비교,ALI조、L-PHC조화H-PHC조폐조직함수량、BALF단백농도승고,폐조직Ang-1화린산화Tie-2표체하조(P＜0.05)；여ALI조비교,H-PHC조폐조직함수량、BALF단백농도강저,폐조직Ang-1화린산화Tie-2표체상조(P＜0.05),L-PHC조상술지표차이무통계학의의(P＞0.05).H-PHC조폐조직손상교ALI조감경.결론 염산무을규미가개선폐혈관배통투성,감경폐포상피병장손상,종이감경대서내독소성급성폐손상,차해작용여제량유관,기궤제여상조Ang-1표체화증강Tie-2활성유관.
Objective To evaluate the effect of penehyclidine hydrochloride (PHC) on the level of angiopoietin-1 (Ang-1) and tyrosine kinase receptor-2 (Tie-2) during endotoxin-induced acute lung injury (ALI) in rats.Methods Forty adult male Sprague-Dawley rats,weighing 180-220 g,were randomly divided into 4 groups using a random number table (n =10 each):control group (group C),ALI group,low-dose PHC group (group L-PHC) and high-dose PHC group (group H-PHC).ALI was induced with iv injection of lipopolysaccharide 5.0 mg/kg via the tail vein.In L-PHC and H-PHC groups,PHC 0.6 and 2 mg/kg were injected,respectively,via the tail vein at 1 and 24 h after lipopolysaccharide injection.The rats were sacrificed at 48 h after the initial injection of PHC to measure the lung water content,protein concentration in bronchoalveolar lavage fluid (BALF),and the expression of Ang-1,Tie-2 and phosphorylated Tie-2 in lung tissues.The morphological changes of lung tissues were observed under light microscope and the ultrastructural changes of alveolar epithelial barrier under transmission electron microscope.Results Compared with group C,the lung water content and protein concentrations in BALF were significantly increased,and the expression of Ang-1 and phosphorylated Tie-2 was down-regulated in the other three groups (P ＜ 0.05).Compared with group ALI,the lung water content and protein concentrations in BALF were significantly decreased,and the expression of Ang-1 and phosphorylated Tie-2 was up-regulated in H-PHC group (P ＜ 0.05),and no significant changes were found in the parameters mentioned above in group L-PHC (P ＞0.05).The damage to lung tissues was significantly reduced in group H-PHC as compared with group ALI.Conclusion PHC can improve the permeability of pulmonary microvascular and reduce injury to alveolar epithelial barrier,thus ameliorating endotoxin-induced ALI in rats,and the effect is dose-related and up-regulation of Ang-1 expression and inhancement of Tie-2 activity are involved in the mechanism.
