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Updated: Dec 18, 2025

Acute Myocardial Infarction in Rats
Published on: February 16, 2011
[Endoplasmic Reticulum Stress and Mitochondrial Damage in Rat Cardiomyocytes after Acute Myocardial Infarction]
Li He1, Chao-Yi Qin1, Jun Shi1
1Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu 610041, China.
Objective:
To study the alterations of endoplasmic reticulum (ER) stress and mitochondrial damage after acute myocardial infarction (AMI).
Methods:
A total of 40 SD rats were used in this study and 32 of them were subjected to AMI by ligation of left anterior descending artery. The rats were sacrificed and the heart tissues were collected after 1 h, 2 h, 4 h and 6 h of AMI ( n=8 per group). The mRNA levels of activating transcription factor 6 alpha ( ATF6) and immunoglobulin heavy chain binding potein ( BiP), as well as the expression of mitochondrial DNA (mtDNA) in cytoplasm were detected by RT-PCR. The ATP levels in the cardiomyocytes were detected by a commercial ATP assay kit.
Results:
The mRNA levels of ATF6 and BiP were significantly increased after 1 h of AMI, which were maintained at high level from 2 h of AMI to the end of the experiment ( P<0.05). The ATP concentrations in the cardiomyocytes were significantly elevated after 1 h of AMI but remarkably decreased after 4 h and 6 h of AMI ( P<0.05). The release of mtDNA in cytoplasm was significantly increased after 2 h of AMI, followed by further elevations at 4 h and 6 h after AMI ( P<0.05).
Conclusion:
Mitochondrial damage is secondary to ER stress in AMI.
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