A late increase in free radical activity post myocardial infarction.
Free radicals (FR) are a highly reactive chemical species which have been implicated in the pathogenesis of reperfusion injury. Experimental models of reperfusion injury have demonstrated that FR scavengers improve myocardial salvage and thus it has been postulated that they may be of benefit in acute myocardial infarct (MI) patients treated with thrombolysis. Previous studies of FR activity post MI have focused on the immediate post reperfusion period; the present study investigates FR activity in post MI patients over a longer time span. Free radicals have a very short half-life and in clinical studies their activity is usually assessed indirectly by measuring either the level of FR reaction products such as malondialdehyde (MDA) or FR scavengers such as plasma thiols (PSH). In the presence of increased FR activity MDA levels increase and PSH levels decrease. Twenty-two acute MI patients had blood samples taken on admission, day 7 and day 21 post MI for measurement of MDA and PSH levels. On day 7 post MI a significant increase in MDA was detected P = 0.0001 (Sign test) (median change +2.1 mumol.l) and a significant decrease was detected in PSH P = 0.04 (Sign test) (median change, -38 mumol.l-1). No significant differences were detected between admission and day 21 levels of MDA and PSH. This study demonstrates the presence of enhanced FR activity at a later time point than has previously been recognised. White blood cells utilise FRs during phagocytosis and the late rise in FR activity detected in this study may reflect white blood cell removal of necrotic myocardium.
D000328:Adult; D000368:Aged; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D006207:Half-Life; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects / Q000502:physiology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013438:Sulfhydryl Compounds / Q000097:blood; D015912:Thrombolytic Therapy
D017382:Reactive Oxygen Species; D013438:Sulfhydryl Compounds; D008315:Malondialdehyde; D003402:Creatine Kinase