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| Comparison of three rat models of coronary microvascular dysfunction induced by sodium laurate |
| ZHU Jinxian FAN Yawen GONG Shenglan ZHUANG Yuanfei LIU Chungui TANG Xinzheng |
| Department of Cardiovascular Diseases, the Sixth Clinical Medical College of Guangzhou University of Chinese Medicine Shenzhen Hospital of Guangzhou University of Chinese Medicine (Futian), Guangdong Province, Shenzhen 518034, China |
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Abstract Objective To evaluate the optimal scheme of three coronary microcirculation dysfunction models in SD rats induced by sodium laurate. Methods A total of 50 male SD rats aged 6-8 weeks were divided into blank group, sham operation group, and model group 1-3 by random number table method, with ten rats in each group. The blank group did not receive any intervention; in model group 1, the heart was extruded after intercostal expansion and sodium laurate (1 mg/kg) was injected into the apex of the heart once; in model group 2, the heart was extruded after intercostal expansion and sodium laurate (1 mg/kg) was injected into the apex of the heart twice; in model group 3, the heart was extruded after intercostal expansion, the aortic root was clipped and the apex of the heart was injected with sodium laurate (1 mg/kg) once; the sham operation group performed the same operation as model group 2, but the same amount of normal saline was injected. Echocardiogram was used to evaluate cardiac function after 72 h of continuous feeding. The pathological changes of myocardial tissue were observed by HE staining, Heidenhain staining, and Carstairs staining. Results The mortality rate of operational rats was 17.5% (7/40). There was no significant difference in left ventricular ejection fraction (LVEF) between sham operation group and blank group (P > 0.05). Compared with the sham operation group, the LVEF of the model group 1-3 was decreased (P < 0.05); compared with model group 2, LVEF in model group 1 and 3 was increased (P < 0.05). HE staining showed that myocardial cell lysis, rupture, and inflammatory cell infiltration, coronary microvascular thrombosis in different degrees were observed in model group 1-3. Heidenhain staining showed that different degrees of dot, sheet, and mass black staining could be seen in the myocardial fibers of model group 1-3. Carstairs staining showed that purple thrombus which consists of overlapping platelets and fibrin could be seen in the coronary microvascular of model group 1-3. Conclusion Three modeling methods can establish the model of coronary microvascular dysfunction, and the model established by squeezed out the heart after expanding the intercostal space and injecting sodium laurate (1 mg/kg) into the apex twice is more stable and reliable.
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