Distribution of fibrinogen and albumin in normal, ischaemic, and necrotic myocardium during the evolution of myocardial infarction: an immunohistochemical study.
The role of mediators of inflammation in the pathogenesis and evolution of myocardial infarction has attracted increased interest as interventions which inhibit the inflammatory response after coronary artery occlusion have been shown to decrease infarct size. The distribution of fibrinogen and albumin in ischaemia myocardium after closed chest balloon occlusion of the left anterior descending coronary artery was studied by immunohistochemical techniques in 34 dogs, and compared to morphological evaluation of cellular injury. In myocardium which was ischaemic but not necrotic (that is, glycogen loss and the absence of light and electron microscopic and tetrazolium staining evidence of necrosis, n = 8 dogs) no accumulation of these proteins was detected within the ischaemic zone. In myocardium which was necrotic by morphological criteria (n = 26 dogs), fibrinogen and albumin were detected in the necrotic fibres as early as 3 h after coronary occlusion using both the peroxidase-antiperoxidase and avidin-biotin immunostaining methods. Non-ischaemic myocardium never showed positive staining. The presence of fibrinogen and albumin in myocardial fibres appears to be specific for indicating irreversible injury.
D000418:Albumins / Q000032:analysis*; D000818:Animals; D003331:Coronary Vessels; D004285:Dogs; D005340:Fibrinogen / Q000032:analysis*; D007158:Immunologic Techniques; D007511:Ischemia / Q000378:metabolism; D009203:Myocardial Infarction / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000032:analysis* / Q000276:immunology / Q000473:pathology; D009336:Necrosis
D000418:Albumins; D005340:Fibrinogen