Immunohistochemical alterations after intravital and post-mortem traumatic myocardial damage.
Two series of experiments have been carried out on heart tissue for the occurrence of post-mortem and intravital myocardial damage. The first series was carried out on 18 porcine hearts collected immediately after the pigs were killed in a slaughterhouse. The hearts were subjected to stab wounds post-mortem, varying between 5 min and 140 min after death. The second series investigated were human hearts with intravital damage, i.e. 4 stab wounds, 1 gunshot, 13 contusions and ruptures. The time the trauma occurred before death varied between 0 and 30 min. The investigation comprised the four myocyte structural proteins myoglobin, FABP, troponin C, desmin and the three plasma proteins fibrinogen, fibronectin and C5b-9. Both series exhibited a variety of direct traumatic changes with a much broader zone in vital damage compared to post-mortem damage. In vital damage the zone of direct damage is in continuity with a further zone of indirect damage which is a three dimensional network. The signs of damage are contraction bands, depletion of structure antigens, contraction-associated accumulation of structure proteins, accumulation of plasma proteins on the cell surfaces and in the interstitium. In vital damages there is in addition an intrasarcolemmal accumulation of plasma proteins. The pattern of all damage is much broader and much more variegated in vital damage, thus vital damage can be clearly differentiated from post-mortem damage. bin, heart-type fatty acid binding protein (FABP), troponin, desmin, fibrinogen and fibronectin (Amberg 1995; Brinkmann et al. 1993; Glatz et al. 1994; Kleine et al. 1993; Leadbetter et al. 1989; Ortmann et al. 2000a, 2000b; Osuna et al. 1998; Thomsen and Held 1994, 1995). The aim of the present study was to elaborate reaction patterns of these marker proteins in mechanical heart trauma induced ante- and post-mortem and to explore their value for wound age determination in forensic casework.
Ortmann
C
C
Institut für Rechtsmedizin, Westfälische Wilhelms-Universität, Münster, Germany.
Pfeiffer
H
H
Brinkmann
B
B
D000293:Adolescent; D000328:Adult; D000368:Aged; D000818:Animals; D001798:Blood Proteins / Q000378:metabolism; D002352:Carrier Proteins / Q000378:metabolism; D003893:Desmin / Q000378:metabolism; D000071438:Fatty Acid-Binding Protein 7; D050556:Fatty Acid-Binding Proteins; D005260:Female; D005554:Forensic Medicine; D006335:Heart Injuries / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D009211:Myoglobin / Q000378:metabolism; D009363:Neoplasm Proteins; D011180:Postmortem Changes; D013552:Swine; D019209:Troponin C / Q000378:metabolism; D025521:Tumor Suppressor Proteins
D001798:Blood Proteins; D002352:Carrier Proteins; D003893:Desmin; C107608:FABP7 protein, human; D000071438:Fatty Acid-Binding Protein 7; D050556:Fatty Acid-Binding Proteins; D009211:Myoglobin; D009363:Neoplasm Proteins; D019209:Troponin C; D025521:Tumor Suppressor Proteins