title: Characterization of the structural and functional changes in the myocardium following focal ischemia-reperfusion injury.
abstract: High-resolution (11.7 T) cardiac magnetic resonance imaging (MRI) and histological approaches have been employed in tandem to characterize the secondary damage suffered by the murine myocardium following the initial insult caused by ischemia-reperfusion (I/R). I/R-induced changes in the myocardium were examined in five separate groups at the following time points after I/R: 1 h, day 1, day 3, day 7, and day 14. The infarct volume increased from 1 h to day 1 post-I/R. Over time, the loss of myocardial function was observed to be associated with increased infarct volume and worsened regional wall motion. In the infarct region, I/R caused a decrease in end-systolic thickness coupled with small changes in end-diastolic thickness, leading to massive wall thickening abnormalities. In addition, compromised wall thickening was also observed in left ventricular regions adjacent to the infarct region. A tight correlation (r2 = 0.85) between measured MRI and triphenyltetrazolium chloride (TTC) infarct volumes was noted. Our observation that until day 3 post-I/R the infarct size as measured by TTC staining and MRI was much larger than that of the myocyte-silent regions in trichrome- or hematoxylin-eosin-stained sections is consistent with the literature and leads to the conclusion that at such an early phase, the infarct site contains structurally intact myocytes that are functionally compromised. Over time, such affected myocytes were noted to structurally disappear, resulting in consistent infarct sizes obtained from MRI and TTC as well as trichrome and hematoxylin-eosin analyses on day 7 following I/R. Myocardial remodeling following I/R includes secondary myocyte death followed by the loss of cardiac function over time.
authors: Department of Surgery, Davis Heart and Lung Research Institute, The Ohio State University Medical Center, Columbus, OH, USA.
authors: Navdeep
authors: N
authors: Ojha
authors: Sashwati
authors: S
authors: Roy
authors: Jared
authors: J
authors: Radtke
authors: Orlando
authors: O
authors: Simonetti
authors: Surya
authors: S
authors: Gnyawali
authors: Jay L
authors: JL
authors: Zweier
authors: Periannan
authors: P
authors: Kuppusamy
authors: Chandan K
authors: CK
authors: Sen
mesh_terms: D000818:Animals; D001391:Azo Compounds; D016923:Cell Death; D004396:Coloring Agents; D004195:Disease Models, Animal; D004801:Eosine Yellowish-(YS); D006416:Hematoxylin; D008279:Magnetic Resonance Imaging; D008297:Male; D008739:Methyl Green; D051379:Mice; D008810:Mice, Inbred C57BL; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology*; D013194:Staining and Labeling / Q000379:methods; D013778:Tetrazolium Salts; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D001391:Azo Compounds; D004396:Coloring Agents; D013778:Tetrazolium Salts; C017768:trichrome stain; C009591:triphenyltetrazolium; D008739:Methyl Green; D004801:Eosine Yellowish-(YS); D006416:Hematoxylin