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作 者:曾春来[2] 夏良[1] 马彩艳[1] 刘善宽[1] 胡晓晟[1] 王兴祥[1] 陈君柱[1]
机构地区:[1]浙江大学医学院附属第一医院心内科,杭州310003 [2]浙江省丽水市中心医院
出 处:《中华结核和呼吸杂志》2008年第5期330-334,共5页Chinese Journal of Tuberculosis and Respiratory Diseases
摘 要:目的 观察脱氢野百合碱(DHMC)诱发犬肺动脉高压形成前后循环内皮祖细胞数量和功能的变化。方法10只Beagle犬经右心室注射DHMC诱导肺动脉高压(PAH)。注射DHMC前、注射后6周采集静脉血,用流式细胞仪分析AC133和KDR检测双阳性的细胞数量。收集单个核细胞体外培养7d后进行乙酰化低密度脂蛋白胆固醇(DiLDL)摄取和凝集素-I(UEA-I)结合反应,并进行体外血管生成试验。计量资料采用孟x±s表示,采用配对t检验进行统计学分析。结果 10只Beagle犬注射DHMC后9只存活,1只于第2天死亡。注射DHMC后6周肺动脉平均压由(11.3±2.0)mm Hg(1 mm Hg=0.133 kPa)增高到(20.2±1.6)mm Hg(t=10.307,P〈0.01)。PAH形成前后经流式细胞仪分析的AC133和KDR双阳性细胞数量分别为(632.8±42.8)个/ml和(206.1±26.8)个/ml(t=25.361,P〈0.01);体外培养7d的细胞中UEA-I和DiLDL染色双阳性细胞数量分别为(41±6)个/200倍视野和(22±6)个/200倍视野(t=6.510,P〈0.01)。体外成血管试验中形成的血管数为(21.1±2.8)支/200倍视野和(11.2±2.8)支/200倍视野(t=7.583,P〈0.01)。结论 犬肺动脉高压形成后循环内皮祖细胞数量减少,成血管能力下降。Objective To detemfine the quantitive and functional changes of circulating endothelial progenitor cells (EPCs) in dogs with dehydromonocrotaline-induced pulmonary artery hypertension (PAH). Methods Dehydromonocrotaline was injected into the canine right ventricle to induce pulmonary hypertension. Circulating EPCs were enumerated as AC^+133, KDR^+ cells by fluorescence-activated cell sorter using counting beads, and the number and activity of EPCs after in vitro expansion were determined by acLDL uptake/lectin staining assay and in vitro tubule forming assay. Results Nine of the 10 beagles survived after dehydromonocrotaline injection. Six weeks later, mean pulmonary artery pressure increased from (11.3 ±2.0) mm Hg(1 mm Hg= 0. 133 kPa) to (20.2±1.6) mm Hg (t =10.307, P〈0.01), and the AC^+133 and KDR^+ cells decreased from (632. 8 ±42. 8) cells/ml to (206. 1±26. 8) cells/ml (t = 25. 361, P 〈0. 01 ). UEA-I and DiLDL positive cells deceased from (41±6) EPC8/×200 field to (22±6) EPCs/×200 field (t =6. 510, P 〈0. 01 ). In addition, in vasculogenesis assay, PAH EPCs formed less quantitative ( 11.2 ± 2. 8 vs 21.1 ± 2. 8 tubules/×200 field, respectively, t = 7. 583, P 〈 0. 01 ) and less qualitive tubules than baseline EPCs. Conclusion The number and vessel forming ability of EPCs are impaired in this canine model of dehydromonocrotaline-induced pulmonary hypertension.
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