Free Radicals And Myocardial Injury

Abstract

An imbalance between myocardial oxygen and substrate demand and supply leads to ischemia. For many years, it was believed that reperfusion of ischemic myocardium led to the recovery of reversibly injured cells and to the death of irreversibly injured tissue. Over the last 15 years evidence has accumulated that this may not be true and that reperfusion may harm as well as benefit ischemic myocardium a “double edged sword”.

Singlet oxygen is also not a free radical but it can interact with substances to produce free radicals. The superoxide radical (O2.) is formed by the addition of an electron to molecular oxygen. It is formed in almost aflaerobic cells and is one of the mechanisms by which phagocyte cells (neutrophils, monocytes, macmph- ages and eosinophils) act. Superoxide reacts, viaseve ral stages, with hydrogen ions to form hydrogen peroxide [1].

Thirty minutes of ischemia results in an increase in xanthenes oxides activity from the baseline 6-10% up to 27-33% of the total activity 8,10, most of the converse ion occurs in the first 5 minutes of ischaemia8.

Catecholamine metabolism Catecholamines are released in response to ischemia and their degrade ion, by monoamine oxides, may produce hydroxyl radicals’8. The significance of this pathway in reperfus ion injury is unknown.

It appears that oxygen-derived free radicals are almost certainly involved in the injui occurring to ischemic myocardium upon reperfusion. Where the most significant damage occurs (endothelium, cell membrane etc.) remains to be defined and whether the pattern of injury differs in different settings (eg, regional and global ischemia/reperfusion) is also unclear. Free radical scavengers appear to have a part to play in preventing or ameliorating the damage of reperfusion but the dosage of the agents, the method of administration and the timing of delivery remain to be defamed before they can be adopted clinically.