H-X Chang1, X-J Zhao2, Q-L Zhu2, Q Hou3, Y Li4. 1. Emergency Department, Children's Hospital of Hebei Province, Shijiazhuang, Hebei, China. 2. Department of Cardiology, General Hospital of Chinese People's Liberation Army, No. 28 Fuxing Road, 100853, Haidian District, Beijing, China. 3. Institute of Basic Medicine, General Hospital of Chinese People's Liberation Army, Haidian District, Beijing, China. 4. Department of Cardiology, General Hospital of Chinese People's Liberation Army, No. 28 Fuxing Road, 100853, Haidian District, Beijing, China. liyangxys@163.com.
Abstract
BACKGROUND: The aim of this study was to assess the role of lipolysis of epicardial adipose tissue (EAT) in cardiac function after myocardial infarction (MI). METHODS: We used a rat model of MI with or without EAT removal to study the effects of EAT lipolysis on cardiovascular function. Echocardiography and cardiac catheterization were used to determine cardiac function, and infarct size and histopathology specimens were analyzed in postmortem sections. Inflammatory responses were evaluated via flow cytometry and Elisa analyses. RESULTS: We found that the lipolysis of EAT increased significantly after MI. Removal of the EAT after MI (MI-EAT) improved cardiac function by nearly 10% and decreased the infarct area by 6% when compared with rats retaining EAT after MI (MI+EAT). Furthermore, the removal of EAT reduced the number of CD45-positive leukocytes (50 vs. 34.8%) and increased the ratio of macrophage/leukocytes (56 vs. 75%) in the infarcted heart. Compared with the MI+EAT group, the concentration of tumor necrosis factor-alpha and interleukin 1‑beta were reduced in the MI-EAT group. CONCLUSION: Lipolysis of EAT increased significantly after MI. Removal of EAT improved cardiac function, in part, by weakening the inflammatory response.
BACKGROUND: The aim of this study was to assess the role of lipolysis of epicardial adipose tissue (EAT) in cardiac function after myocardial infarction (MI). METHODS: We used a rat model of MI with or without EAT removal to study the effects of EAT lipolysis on cardiovascular function. Echocardiography and cardiac catheterization were used to determine cardiac function, and infarct size and histopathology specimens were analyzed in postmortem sections. Inflammatory responses were evaluated via flow cytometry and Elisa analyses. RESULTS: We found that the lipolysis of EAT increased significantly after MI. Removal of the EAT after MI (MI-EAT) improved cardiac function by nearly 10% and decreased the infarct area by 6% when compared with rats retaining EAT after MI (MI+EAT). Furthermore, the removal of EAT reduced the number of CD45-positive leukocytes (50 vs. 34.8%) and increased the ratio of macrophage/leukocytes (56 vs. 75%) in the infarcted heart. Compared with the MI+EAT group, the concentration of tumor necrosis factor-alpha and interleukin 1‑beta were reduced in the MI-EAT group. CONCLUSION: Lipolysis of EAT increased significantly after MI. Removal of EAT improved cardiac function, in part, by weakening the inflammatory response.
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