The myocardial protective effect of propofol on rats with experimental myocardial infarction and its mechanism.
- Author:
Ming-Xiao ZHANG
1
;
Qing-Xin TIAN
2
;
Jian-Long LIU
2
Author Information
1. Department of Anesthesiology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China. zmxmzk@126.com.
2. Department of Anesthesiology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Cardiotonic Agents/pharmacology*;
Matrix Metalloproteinase 2;
Matrix Metalloproteinase 9;
Myocardial Infarction/drug therapy*;
Myocardium;
Propofol/pharmacology*;
Rats;
Tissue Inhibitor of Metalloproteinase-2/genetics*;
Ventricular Remodeling
- From:
Acta Physiologica Sinica
2021;73(6):878-884
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the present study was to investigate the protective effect of propofol on the experimental myocardial infarction in rats. The myocardial infarction model was established by ligating the anterior descending branch of left coronary artery in rats. Model rats were treated with propofol. Cardiac function was evaluated by echocardiography. Cardiac hemodynamic changes were detected by multiconductor biorecorder. Pathological changes in the infarcted myocardia were detected by HE staining. The expression levels of cardiac hypertrophy marker genes and fibrosis marker proteins were analyzed by real-time quantitative PCR and Western blot. The results showed that, compared with the sham surgery group, the model group exhibited larger infarct size (> 40%), impaired heart function, and significantly increased left ventricular end-diastolic pressure (LVEDP). Propofol reduced cardiac function impairment and decreased LVEDP in the model group. Propofol significantly reduced lung weight/body weight ratio, heart weight/body weight ratio, left ventricular weight/body weight ratio and left atrial weight/body weight ratio in the model group. Furthermore, after myocardial infarction, the administration of propofol significantly improved the diastolic strain rate, down-regulated the mRNA expression levels of myocardial hypertrophy markers, atrial natriuretic peptide and β-myosin heavy chain, and reversed the up-regulation of matrix metalloproteinase 2 (MMP2), MMP9 and tissue inhibitor of metalloproteinase-2 (TIMP-2) induced by myocardial infarction. These results suggest propofol can reduce adverse ventricular remodeling, cardiac dysfunction, myocardial hypertrophy and fibrosis after myocardial infarction, and has protective effect against the experimental myocardial infarction induced by coronary artery ligation in rats.
