title: Ischemia and reperfusion of the porcine myocardium: effect on collagen.
abstract: We studied the effect of acute myocardial infarction and late reperfusion on myocardial collagen in a closed chest porcine model, to investigate if any collagen degradation could be detected in blood samples and myocardium. Sixteen 60-80 kg pigs were used with six animals serving as controls and 10 submitted to ischemia-reperfusion. In the ischemia-reperfusion group the left anterior descending coronary artery was occluded for 6 h by inflation of a percutaneous transluminal coronary angioplasty balloon followed by reperfusion for 3 h. Blood samples were taken from the aorta and the coronary sinus and analyzed for creatine kinase and collagen degradation products, i.e. the N-terminal propeptide of procollagen type III (PIIINP) and C-terminal pyridinoline cross-linked telopeptide of collagen type I (ICTP). Myocardial tissue samples were analyzed for content of hydroxyproline, collagen volume fraction and amount of extractable PIIINP/dry weight. Transmission electron microscopy of biopsies was performed to evaluate myocytes and collagen structure outside and within the infarct zone. Creatine kinase showed a statistically significant increase during ischemia and reperfusion but we found no evidence of release of collagen degradation products either during ischemia or reperfusion compared with control. Myocardial content of hydroxyproline, collagen volume fraction and extractable PIIINP/dry weight did not differ between groups. Transmission electron microscopy of biopsies from the infarct zone showed myocyte damage but no visible evidence of collagen degradation when photos were evaluated blindly. In this porcine model of acute myocardial infarction and late reperfusion no release of collagen degradation products from the myocardium or any decrease in or damage to myocardial collagen was detected.
authors.affiliation: Department of Cardiology, Skejby Sygehus, Aarhus University Hospital, Denmark.
authors.forename: H
authors.initials: H
authors.lastname: Wiggers
authors.forename: T
authors.initials: T
authors.lastname: Klebe
authors.forename: L
authors.initials: L
authors.lastname: Heickendorff
authors.forename: N B
authors.initials: NB
authors.lastname: Høst
authors.forename: C C
authors.initials: CC
authors.lastname: Danielsen
authors.forename: U
authors.initials: U
authors.lastname: Baandrup
authors.forename: H R
authors.initials: HR
authors.lastname: Andersen
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D015415:Biomarkers / Q000097:blood; D003094:Collagen / Q000097:blood / Q000378:metabolism*; D024042:Collagen Type I; D003402:Creatine Kinase / Q000097:blood; D004195:Disease Models, Animal; D006439:Hemodynamics / Q000502:physiology; D006909:Hydroxyproline / Q000378:metabolism; D008854:Microscopy, Electron; D009203:Myocardial Infarction / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury; D009206:Myocardium / Q000378:metabolism*; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides / Q000097:blood; D011347:Procollagen / Q000097:blood; D013552:Swine
chemical_list: D015415:Biomarkers; D024042:Collagen Type I; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; C041876:procollagen Type III-N-terminal peptide; D003094:Collagen; D003402:Creatine Kinase; D006909:Hydroxyproline