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Updated: Jun 12, 2026

Simultaneous Isolation of High Quality Cardiomyocytes, Endothelial Cells, and Fibroblasts from an Adult Rat Heart
Published on: May 19, 2017
Cardioprotection and ageing
1Department of Anesthesiology and Pain Medicine and Anaesthesia and Pain Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Abstract:
With an increase in the elderly population and an increase in the prevalence of age-related cardiovascular disease, anesthesiologists are increasingly being faced with elderly patients with known or suspected ischemic heart disease in the perioperative period. Although early reperfusion remains the best strategy to reduce ischemic injury, reperfusion may damage the myocardium. Adjuvant therapy to revascularization is therefore necessary. To develop better strategies to prevent ischemia-reperfusion injury in older patients, we need to understand the aged myocardium, which has undergone structural and functional changes relative to the normal myocardium, resulting in reduced functional capacity and vulnerability to ischemia-reperfusion injury. In addition, innate or acquired cardioprotection deteriorates with aging. These changes in the aged myocardium might explain why there is poor translation of basic research findings from young animals to older patients. In this review, I discuss changes in intracellular signaling associated with myocardial ageing that have an effect on ischemia-reperfusion injury, and I discuss the efficacy of cardioprotection afforded by ischemic and pharmacologic pre-and post-conditioning in the aged myocardium. Finally, I outline strategies to restore protection in the aged myocardium.
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