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作 者:田晨光[1,2,3] 李鹏诺[1,2,3] 曹清云[1,2,3] 董义光[1,2,3]
机构地区:[1]河南医科大学第二附属医院内分泌科 [2]商丘地区医院内科 [3]河南医科大学第一附属医院
出 处:《河南医学研究》1997年第4期301-303,共3页Henan Medical Research
摘 要:目的:通过心肌超微结构的治疗观察,探讨心肌病变的发病机理,为临床治疗做有益的探索。方法:Aloxan诱发糖尿病大白鼠并检测血脂、血栓素和前列环素代谢产物水平,电子显微镜观察坐骨神经超微结构。结果:蝮蛇抗栓酶可显著降低糖尿病大鼠第22周时血TG(P<0.05)和TC水平,降低血栓素与前列环素的比值,达到了降血脂、改善微循环的目的。但是,糖尿病大鼠两组间心肌超微结构病理变化无明显差异,均可见肌小节结构紊乱,闰盘间隙增宽,肌原纤维变性,线粒体代偿性增生,肿胀变性、嵴变短、膜破裂。细胞内脂滴积聚,糖原颗粒沉积。结论:单纯的降血脂、改善微循环治疗不能有效阻止心肌病变的发生。文章对结果及心肌病变的发生机理进行了讨论。Objective: To observe the myocardial ultrastructure of diabetic cardiomyopathy and probe its pathogenesis and therapeutic method.Methods: The study had been carried out on the model of alloxan induced diabetic rats.The diabetic treatment group(DT) was given Ahylysantinfarctase.Then,the triglyceride(Tg),total cholesterol (Tc),high density lipoprotein cholesterol(HDL-C) and degraded product of thomboxane and prostacyclin are examined in different period.The myocardial ultrastructure was also observed. Results: The level of Tg was increased and HDL-C was decreased significantly in 22-week diabetic control group(DC) than that in DT group ( P <0.05).The ratio of TXB 2 and 6-keto-PGF 1α was reduced effectively.The observation of myocardial ultrastructure showed myoarchitectonic derangement of typical myocardial myocomma,shortened parazone,widened space between intercalated disks,myofibrillar degeneration fragmentation and vacuolization,mitochondrial compensatory proliferation swelling shortened crista and rhegma of membrane,lipid droplets and glycogen granule could be seen in the cytoplasm of cardiac myocytes.But,the ultrastructural changes didnt have discrepancy between DC and DT. Conclution:The paper analyse the reason of leading to those manifestation.The author think that only the amelioration of circulatory factors cant effectively prevent the occurrence of cardiomyopath in diabetic rats.
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