title: Differences in transmural distribution of cardiomyocyte injury Ca paradox versus postischemic reperfusion phenomenon.
abstract: Normothermic, 3 min lasting perfusion of isolated rat heart with Krebs-Ringer-Henseleit solution in which Ca was replaced by EDTA, followed by successive perfusion of Ca2+ containing medium resulted in structural and metabolic derangement of myocardial cells; this could be demonstrated electronmicroscopically and histochemically. Unlike in ischemia, Ca paradox left the enzymes LDH, SDH, beta-HBDH as well as alpha-glucan phosphorylase and ATP-ases better preserved in the subendocardial layer of the left ventricle. Ultrastructural analysis of this phenomenon showed good correlations with the histochemical findings. A large portion of cardiomyocytes in the subendocardial layer showed only slight changes. On the other hand, myocytes in the subepicardial layer were severely injured and all characteristics of the calcium paradox were present including hypercontraction bands with fusion of myofilaments, extrusion and accumulation of oedematous mitochondria containing electron dense material intracristally, sarcolemmal ruptures, separation of intercalated discs etc. The better preservation of the subendocardial region in experiments with calcium paradox could be explained by inadequate perfusion of this layer with Ca2+ free medium due to transmural anatomical inhomogeneity of the capillary supply, resulting in a better protection of these myocytes from Ca paradox. The heterogeneity in transmural distribution of injuries is a multifactorial phenomenon. In addition to factors such as intramural pressure gradient, transmural pressure, enddiastolic intraventricular pressure etc., the most important factors in both types of injuries should be regarded the amount of vascular supply, blood flow and perfusate volume.
authors.affiliation: Institute of Experimental Surgery, Slovak Academy of Sciences, Bratislava, Czechoslovakia.
authors.forename: J
authors.initials: J
authors.lastname: Slezák
authors.forename: N
authors.initials: N
authors.lastname: Tribulová
authors.forename: W
authors.initials: W
authors.lastname: Schulze
authors.forename: A
authors.initials: A
authors.lastname: Ziegelhöffer
authors.forename: T
authors.initials: T
authors.lastname: Ravingerová
authors.forename: J
authors.initials: J
authors.lastname: Okolicány
authors.forename: V
authors.initials: V
authors.lastname: Trégerová
mesh_terms: D000818:Animals; D002118:Calcium / Q000494:pharmacology / Q000502:physiology*; D003327:Coronary Disease / Q000473:pathology / Q000503:physiopathology*; D004492:Edetic Acid / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D008854:Microscopy, Electron; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000648:ultrastructure; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D004492:Edetic Acid; D002118:Calcium