西安交通大学学报(医学版)
西安交通大學學報(醫學版)
서안교통대학학보(의학판)
JOURNAL OF XI'AN JIAOTONG UNIVERSITY(MEDICAL SCIENCES)
2014年
3期
352-356,360
,共6页
李强%冯华%喻安永%陈景宇%赵喆%吴国材%阮怀珍
李彊%馮華%喻安永%陳景宇%趙喆%吳國材%阮懷珍
리강%풍화%유안영%진경우%조철%오국재%원부진
蛛网膜下腔出血%早期脑损伤%微血管痉挛%二乙烯三胺/一氧化氮聚合物(DETA/NO)%一氧化氮
蛛網膜下腔齣血%早期腦損傷%微血管痙攣%二乙烯三胺/一氧化氮聚閤物(DETA/NO)%一氧化氮
주망막하강출혈%조기뇌손상%미혈관경련%이을희삼알/일양화담취합물(DETA/NO)%일양화담
subarachnoid hemorrhage%early brain injury%capillary spasm%diethylenetriamine/nitric oxide (DETA/NO)%nitric oxide
目的:通过二乙烯三胺/一氧化氮聚合物(DETA/NO)对雄性 SD大鼠线穿法建造的蛛网膜下腔出血(SAH)模型的干预,观察其对微血管痉挛的防治及降低早期脑损伤作用。方法将69只雄性 SD 大鼠随机分为假手术组(sham组)、对照组(SAH 组)和治疗组(DETA/NO组)。通过线穿建立 SAH 模型,观察大体动物 Garcia神经功能评分,免疫荧光染色检测微血管肌动蛋白αSMA及PDGFRβ的表达,一氧化氮(NO)试剂盒检测脑组织 NO 浓度变化,观察血红蛋白刺激离体脑片微血管变化情况。结果手术后3 d,DETA/NO 组较 SAH 组神经功能评分明显改善(P <0.05);免疫荧光结果显示,SAH 后大脑皮层微血管周围αSMA、PDGFRβ表达上调(P <0.05),DETA/NO 能在一定程度上逆转此过程(P<0.05);术后SAH 3 h左右NO浓度显著降低(P<0.05),此后逐渐回升,DETA/NO能在早期维持 NO浓度(P <0.05);观察到脑片皮层微血管受血红蛋白刺激收缩,DETA/NO 能缓解微血管痉挛。结论 DETA/NO能降低大鼠蛛网膜下腔出血后微血管痉挛及早期脑损伤。
目的:通過二乙烯三胺/一氧化氮聚閤物(DETA/NO)對雄性 SD大鼠線穿法建造的蛛網膜下腔齣血(SAH)模型的榦預,觀察其對微血管痙攣的防治及降低早期腦損傷作用。方法將69隻雄性 SD 大鼠隨機分為假手術組(sham組)、對照組(SAH 組)和治療組(DETA/NO組)。通過線穿建立 SAH 模型,觀察大體動物 Garcia神經功能評分,免疫熒光染色檢測微血管肌動蛋白αSMA及PDGFRβ的錶達,一氧化氮(NO)試劑盒檢測腦組織 NO 濃度變化,觀察血紅蛋白刺激離體腦片微血管變化情況。結果手術後3 d,DETA/NO 組較 SAH 組神經功能評分明顯改善(P <0.05);免疫熒光結果顯示,SAH 後大腦皮層微血管週圍αSMA、PDGFRβ錶達上調(P <0.05),DETA/NO 能在一定程度上逆轉此過程(P<0.05);術後SAH 3 h左右NO濃度顯著降低(P<0.05),此後逐漸迴升,DETA/NO能在早期維持 NO濃度(P <0.05);觀察到腦片皮層微血管受血紅蛋白刺激收縮,DETA/NO 能緩解微血管痙攣。結論 DETA/NO能降低大鼠蛛網膜下腔齣血後微血管痙攣及早期腦損傷。
목적:통과이을희삼알/일양화담취합물(DETA/NO)대웅성 SD대서선천법건조적주망막하강출혈(SAH)모형적간예,관찰기대미혈관경련적방치급강저조기뇌손상작용。방법장69지웅성 SD 대서수궤분위가수술조(sham조)、대조조(SAH 조)화치료조(DETA/NO조)。통과선천건립 SAH 모형,관찰대체동물 Garcia신경공능평분,면역형광염색검측미혈관기동단백αSMA급PDGFRβ적표체,일양화담(NO)시제합검측뇌조직 NO 농도변화,관찰혈홍단백자격리체뇌편미혈관변화정황。결과수술후3 d,DETA/NO 조교 SAH 조신경공능평분명현개선(P <0.05);면역형광결과현시,SAH 후대뇌피층미혈관주위αSMA、PDGFRβ표체상조(P <0.05),DETA/NO 능재일정정도상역전차과정(P<0.05);술후SAH 3 h좌우NO농도현저강저(P<0.05),차후축점회승,DETA/NO능재조기유지 NO농도(P <0.05);관찰도뇌편피층미혈관수혈홍단백자격수축,DETA/NO 능완해미혈관경련。결론 DETA/NO능강저대서주망막하강출혈후미혈관경련급조기뇌손상。
Objective To explore the effects of diethylenetriamine/nitric oxide (DETA/NO)on capillary spasm and early brain injury (EBI)after subarachnoid hemorrhage (SAH)in rats.Methods Sixty-nine male Sprague-dawley rats were randomized into three groups:sham group,SAH group and DETA/NO group.SAH model was established by wearing out the willis ring with thread and then Garcia neurological score was observed in the general animals.The expressions of alpha smooth muscle actin (αSMA)and PDGFRβwere detected by dual immunofluorescence staining;nitric oxide kit was used for detecting brain tissue NO concentration.Changes in the hemoglobin-stimulated capillaries were observed in rat slices.Results Three days after surgery,neurological deficit score was remarkably improved in DETA/NO group compared with that in SAH group (P<0 .0 5 ). Immunofluorescence results showed that the expressions of peri-capillaryαSMA and PDGFRβwere significantly increased after SAH (P<0.05 ),and that DETA/NO could down-regulate the expressions (P<0.05 ).NO concentration was greatly reduced about 3 hours after SAH and then gradually increased;DETA/NO could maintain the concentration of NO at an early stage (P<0 .0 5 ).The capillary contraction was observed in slices perfused with hemoglobin;DETA/NO could alleviate capillary spasm.Conclusion DETA/NO can alleviate the severity of capillary spasm and EBI after SAH in rats.