Therapeutic strategies for ischemia reperfusion injury in emergency medicine

Abstract

Ischemia reperfusion (IR) injury occurs when blood supply, perfusion, and concomitant reoxygenation is restored to an organ or area following an initial poor blood supply after a critical time period. Ischemia reperfusion injury contributes to mortality and morbidity in many pathological conditions in emergency medicine clinical practice, including trauma, ischemic stroke, myocardial infarction, and post-cardiac arrest syndrome. The process of IR is multifactorial, and its pathogenesis involves several mechanisms. Reactive oxygen species are considered key molecules in reperfusion injury due to their potent oxidizing and reducing effects that directly damage cellular membranes by lipid peroxidation. In general, IR injury to an individual organ causes various pro-inflammatory mediators to be released, which could then induce inflammation in remote organs, thereby possibly advancing the dysfunction of multiple organs. In this review, we summarize IR injury in emergency medicine. Potential therapies include pharmacological treatment, ischemic preconditioning, and the use of medical gases or vitamin therapy, which could significantly help experts develop strategies to inhibit IR injury.

Luminal preloading with hydrogen‐rich saline ameliorates ischemia‐reperfusion injury following intestinal transplantation in rats

“…Hydrogen represents an effective and non‐toxic molecule with wide potential for treating various diseases associated with oxidative injury, including transplantation‐related organ damage 24,25 . Protective mechanisms have not been fully elucidated.…”

Could Ergothioneine Aid in the Treatment of Coronavirus Patients?

“…Whether through thrombosis formation or respiratory deficiency, the hypoxic state can lead to organ and tissue injury. Furthermore, the restoration of oxygen to tissues (especially when a patient is placed on mechanical ventilation) can give rise to reperfusion injury [ 76 , 150 ]. A few earlier studies have demonstrated that ET is protective in tissues exposed to ischemia-reperfusion injury.…”

Clinical application of nitric oxide in ischemia and reperfusion injury: A literature review

“…[ 21 ] IRI damage to the microvasculature can continue to reduce blood flow to the ischemic tissue, leading to the “no-reflow phenomenon.”[ 22 ] Many therapies have been introduced to combat IRI including but not limited to edaravone, vitamins, therapeutic hypothermia, and NO. [ 23 ] Studies show that NO and its derivatives such as inhaled NO, nitrites, and peroxynitrite modulate IRI of the myocardium. [ 24 ] For this review, we will examine the various NO derivatives and their efficacy in modulating MIs.…”