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作 者:袁斯明[1] 欧阳天祥[1] 邢新[1] 倪灿荣[2] 郑唯强[2] 温萍[2]
机构地区:[1]解放军第二军医大学长海医院整形外科,上海市200433 [2]解放军第二军医大学长海医院病理科,上海市200433
出 处:《中国临床康复》2005年第14期53-55,i002,共4页Chinese Journal of Clinical Rehabilitation
摘 要:目的:研究内皮细胞、平滑肌细胞在体表海绵状静脉畸形中的分布与表型,并分析其发病机制和研究结果对疾病治疗和功能康复的意义。方法:实验于1996-06/2000-08在第二军医大学整形外科实验室完成。畸形组织25根,正常中小静脉各12根。苏木精-伊红染色观察比较畸形血窦壁和中小静脉壁中内皮细胞、平滑肌细胞的分布并计数分析。Envision法免疫组化染色,观察CD31,α平滑肌肌动蛋白在畸形和中小静脉中的分布。结果:畸形血窦壁中平滑肌细胞数量少,排列紊乱,平滑肌细胞与内皮细胞的比例显著低于微小静脉壁。畸形中CD31表达与中小静脉相似,但α平滑肌肌动蛋白的表达明显低于中小静脉,排列紊乱。结论:海绵状静脉畸形血窦壁中内皮细胞和平滑肌细胞发育不均衡,平滑肌细胞表型异常,导致血窦壁薄弱而在血窦内血液的压力下不断扩张,引起血管塑形障碍,这可能是病变发生和进展的原因。闭塞病理性血窦、阻断病变进展过程从而尽可能保留功能是临床治疗的重点。AIM:To investigate the distribution and phenotype of endothelial cells(ECs) an d smooth muscle cells(SMCs) in malformed cavernous vein of body surface,and anal yze its pathogenesis and the significance to the treatment and the functional re habilitation. METHODS:The experiment was performed in the Laboratory for Plastic Surgery,Sec ond Military Medical University of Chinese PLA from June 1996 to August 2000.Twe nty five pieces of malformed veins,12 pieces of medium veins and 12 pieces of s mall veins were included.Hematoxylin and Eosin(HE) staining was used to observe and compare the distribution of ECs and SMCs,and the number of ECs and SMCs in t he malformed sinusoid wall,medium and small veins was calculated.Envision immuno histochemical staining was applied to investigate the distribution of CD31 and αsmooth muscle actin(α SMA) in malformed,medium and small veins. RESULTS:The SMCs were less and distributed more disorderly in the malformed si nusoid wall,as compared with those in the normal veins,and the ratio of ECs to S MCs of the malformed sinusoid wall was less obviously than of small veins.The ex pression of CD31 in malformed,medium and small veins were similar,but the expres sion of α SMA in the deformed vein was less obviously than that in medium and small ones,and the distribution was more irregular. CONCLUSION:The ECs and SMCs in malformed sinusoid wall develop disproportional ly and the SMCs have an abnormal phenotype.The sinusoid wall becomes so thin tha t it gradually expands under the pressure from the blood in the sinusoid,causing the disability of vascular modeling,which may be the pathologic reason of the o ccurrence and progress of this disease.Occluding the pathologic sinusoid and blo cking its progression to reserve its function as far as possible is the focus of clinical therapy.
分 类 号:R318[医药卫生—生物医学工程]
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