The synchronous mechanism of myocardial regeneration-cell disintegration-myocardial fibrosis and its relationship with heart failure
10.3760/cma.j.issn.1001-4497.2019.10.011
- VernacularTitle: 心力衰竭力学机制研究
- Author:
Hongchao WEI
1
;
Chengxiong GU
1
;
Yang YU
1
;
Chuan WANG
1
;
Mingxin GAO
1
;
Haitao LI
1
;
Jingxing LI
1
Author Information
1. Department of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China
- Publication Type:Journal Article
- Keywords:
Acute myocardial infarction;
Myocardial regeneration;
Fibrillation;
Myocardial tension;
Heart failure
- From:
Chinese Journal of Thoracic and Cardiovascular Surgery
2019;35(10):629-634
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the cardiomyocytes regeneration after myocardial infarction in Chinese small pigs, analyze the mechanism of myocardial fibrosis after myocardial regeneration.
Methods:Nine Chinese small pigs, weight 18-20 kg, 6 pigs in the experimental group(to ligate LAD at the equal blood flow point), and 3 in the control group(no any operation was performed). Monitor the hemodynamics of the left ventricle. Cardiac specimens were taken after 4 weeks of LAD ligation, the left ventricle was divided into 17 segments, and fixed in 4% paraformaldehyde for 1 week. Hematoxylin-Eosin/(HE) staining, PTAH、Ki-67-DAB and α-sarcomeric-actin-DAB staining for pathological observation.
Results:Four weeks of LAD ligation, different range of infarct size could be found in all the 17 segment of left ventricle. There was significant systolic pressure difference between the proximal and distal part in the left ventricular cavity. After 4 weeks of LAD ligation, there were a large number of new cardiomyocytes around the infarction area, which connected with the original mature cardiomyocytes directly. Large number of disassembled cardiomyocytes in the infarcted area and myocardial fibers were broken, cell structure disappeared, and nuclei were scattered in fibrotic tissues.
Conclusion:New cardiomyocytes after myocardial infarction were derived from the mature cardiomyocytes. Myocardial regeneration, cell disintegration, and myocardial fibrosis were performed synchronously under the influence of myocardial tension.
