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作 者:程训民[1] 江时森[1] 马瑞[1] 宫剑滨[1] 周航波[2] 毛广平[2]
机构地区:[1]中国人民解放军南京军区南京总医院心内科,南京210002 [2]中国人民解放军南京军区南京总医院病理科,南京210002
出 处:《微循环学杂志》2008年第1期8-10,F0002,共4页Chinese Journal of Microcirculation
基 金:江苏省六大人才高峰资助项目(编号:2005A6)
摘 要:目的:本研究利用免疫组织化学方法和电镜观察高血压、糖尿病和高血压合并糖尿病对心肌毛细血管周细胞的影响,探讨周细胞在高血压合并糖尿病并发心肌微血管病时的作用。方法:SD大鼠和自发性高血压大鼠(SHR)分别腹腔注射链脲佐菌素结合高能量饲料喂养,复制糖尿病和SHR合并糖尿病模型。动物分为4组:正常SD大鼠组(SD组)、自发性高血压大鼠组(SHR组)、糖尿病组(DM组)与SHR合并DM大鼠组(SHDM组)。16周后透射电镜观察心肌毛细血管周细胞超微结构,α-SMA免疫组织化学染色测定周细胞数量。结果:电镜下,SHR、DM和SHDM组心肌毛细血管周细胞多见,大小不一,胞浆富含细胞器及肌丝,与内皮细胞联系松散。免疫组化结果表明SHR、DM和SHDM组大鼠心肌毛细血管周细胞数均较SD组大鼠显著增多,SHDM组(11.8±3.6)个/视野较SHR组(3.9±1.1)个/视野增多非常显著(P<0.01),但与DM组(10.2±3.3)个/视野比较无显著差异(P>0.05)。结论:高血压合并糖尿病时周细胞表型发生改变,且数量增多,这些变化可能在心肌毛细血管肌化及毛细血管旁纤维化中起重要作用。Objective:To investigate the pathologic changes of the myocardial capillary pericytes in hypertension with diabetes rats.Method:The rat model of hypertensive with diabetes mellitus(SHDM)and the rat model of diabetes mellitus(DM)were induced by an intraperitoneal injection of streptozotocin combined with high fat diet in SD rats and spontaneous hypertensive rats(SHR),respectively.The four groups were as follows:SD,DM,SHR and SHDM.The ultrastructure changes were examined by transmission electron microscope and the number of precity was assessed by immunohistochemistry of ventricular sections at 16 weeks.Results:Ultramicroscopic analysis of capillaries showed the pericytes on myocardial capillaries of SHR,DM,and SHDM were conspicuously abnormal in shape and were with cytoplasm containing abundant myofilament and organelle.In addition,pericytes seemed to be loosely associated with the endothelium.The number of pericytes in SHR,DM and SHDM were significantly increased than that in SD.The number of pericytes in SHDM were much higher than that in SHR(11.8±3.6 vs.3.9±1.1,P<0.01),but no significantly difference than that in DM(11.8±3.6 vs.10.2±3.3,P>0.05).Conclusion:These results suggest the phenotype changes and increase of myocardial capillary pericytes in response to hypertension with diabetes.These changes may contribute to arterializations of myocardial capillary and pericapillary fibrosis.
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