Role of Endothelin-1 on Myocardial Ischemia-Reperfusion Injury: A Comprehensive Review
DOI:
https://doi.org/10.52783/jns.v14.2686Keywords:
Endothelin-1, myocardial ischaemia reperfusion injury, vascular endotheliumAbstract
Background: Effective management of acute myocardial infarction (AMI) relies on the swift restoration of coronary blood flow, yet a significant portion of the myocardium remains underperfused due to ischemia-reperfusion injury (IRI), which is exacerbated by factors such as elevated endothelin-1 (ET-1) levels. The balance between relaxation factors like nitric oxide (NO) and contractile factors is crucial for vascular homeostasis, and any dysregulation in this system can lead to increased myocardial damage and contribute to cardiovascular diseases. Objective: To investigate the impact of endothelin on ischemia-reperfusion injury. Method: The approach adopted is a review of existing literature. This study was designed as a systematic review with a narrative approach to provide ET-1 mechanisms and its contribution to ischaemia-reperfusion myocardial injury. Results: The research indicates that endothelin (ET) plays a significant role in myocardial ischemia and reperfusion, resulting in increased production and release of ET-1. The released ET-1 causes considerable coronary constriction, particularly following ischemia/reperfusion, and may directly contribute to myocardial ischemia while also stimulating neutrophil activation and the formation of free radicals. Studies utilising pharmaceutical agents to block ET-1 actions have demonstrated a decrease in ischemia-reperfusion injury, underscoring the physiological importance of endogenous ET. Nevertheless, conflicting results necessitate further investigation in controlled settings using long-lasting ET receptor antagonists or ET-converting enzyme inhibitors to gain a better understanding of ET's involvement in this scenario. Conclusion: The article highlights that ischaemia and reperfusion significantly influence endothelin (ET) mechanisms, leading to increased production and release of ET-1, which causes coronary constriction and may contribute to ischaemia/reperfusion injury through various pathways. While pharmacological agents targeting ET-1 have shown promise in reducing injury, conflicting results necessitate further research with controlled studies to better understand the role of ET in this context.
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