呋喃唑酮诱发SD大鼠扩张型心肌病病理及神经内分泌研究

Pathological and Neuroendocrinological Study on SD Rat Dilated Cardiomyopathy Animal Model with Furazolidone

目的 :建立一个可靠的、在病理及神经内分泌变化接近于人类扩张型心肌病的动物模型。方法 :选择 4 3只 2周龄SD大鼠喂饲呋喃唑酮 8周 ;检测体重、心脏重量、体表心电图、超声心动图、组织病理及心血管活性肽。结果 :呋喃唑酮组体重减少 ,而心脏重量增加 ;心电图表现为QRS时限与Q -T间期延长 ;心脏超声示LVEDD、LVESD增大 ,而LVEF减小 ;组织病理示心脏重量增加 ,光镜与电镜下表现为典型的扩张型心肌病的病理变化 ;血浆心血管活性肽 :血浆中ANP、AngⅡ、ET和TXB2 增高 ,而PGF1α与血浆PGF1α/TXB2 明显降低。结论 :呋喃唑酮诱发SD大鼠扩张型心肌病动物模型不仅在活体形态学、组织病理而且在神经内分泌方面也与人类相符。

Objective: To establish an animal model of dilated cardiomyopathy (DCM), which is similar with that of human in neuroendocrinology and pathology. Methods:43 two-week SD rats were divided into two groups, which in Furazolidone (Fz) group fed with furazolidone 8 weeks. Body weight (BW), heart weight (HW), electrocardiogram(ECG), echocardiogram(UCG), myocardial pathology and some neuroendocrine factors were detected.Results: The HW /BW ratios were significantly increased ; QRS and Q-T interval were prolonged in Fz group( P <0.05). Echocardiogram showed that LVESD in Fz groups were significantly enlarged compared with those in control group ( P <0.05). The LVEDD showed no difference between the two groups. LVEDD/BW ratios in the Fz groups were significantly increased than those in control, ( P <0.01).The LVEF in Fz groups were significantly declined compared with those in control, ( P <0.001). The pathological findings of heart muscles revealed myocardium derangement, fibrosis and necrosis, which were similar with DCM in human. Meanwhile, the changes of the serum angiotensin II (AngII),endothelin(ET),atriuretic peptide(ANP) ,prost-aglandin F 1α (PGI 2 ),thromboxaneB 2 (TXA 2 ) and the serum PG F 1α /TXB 2 in Fz group were similar with the changes in DCM of human. Conclusion:Fz group had DCM myocardium pathology, neuroendocrine disorders as well as the ECG and UCG changes similar with the characteristics in human DCM 8-week feeding with Fz is the ideal period to develop a DCM animal model.