Myocardial infarction and remodeling in mice: effect of reperfusion

1  DeBakey Heart Center and Department of Medicine, Baylor College of Medicine, Houston, Texas 77030-3498; and 2  Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana 46285 Anatomic and functional changes after either a permanent left anterior descending coronary artery occlusio...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 1999-08, Vol.277 (2), p.H660-H668
Hauptverfasser: Michael, Lloyd H, Ballantyne, Christie M, Zachariah, Justin P, Gould, Kenneth E, Pocius, Jennifer S, Taffet, George E, Hartley, Craig J, Pham, Thuy T, Daniel, Sherita L, Funk, Etai, Entman, Mark L
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Sprache:eng
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Zusammenfassung:1  DeBakey Heart Center and Department of Medicine, Baylor College of Medicine, Houston, Texas 77030-3498; and 2  Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana 46285 Anatomic and functional changes after either a permanent left anterior descending coronary artery occlusion (PO) or 2 h of occlusion followed by reperfusion (OR) in C57BL/6 mice were examined and compared with those in sham-operated mice. Both interventions generated infarcts comprising 30% of the left ventricle (LV) measured at 24 h and equivalent suppression of LV ejection velocity and filling velocity measured by Doppler ultrasound at 1 wk. Serial follow-up revealed that the ventricular ejection velocity and filling velocity returned to the levels of the sham-operated controls in the OR group at 2 wk and remained there; in contrast, PO animals continued to display suppression of both systolic and diastolic function. In contrast, ejection fractions of PO and OR animals were depressed equivalently (50% from sham-operated controls). Anatomic reconstruction of serial cross sections revealed that the percentage of the LV endocardial area overlying the ventricular scar (expansion ratio) was significantly larger in the PO group vs. the OR group (18 ± 1.7% vs. 12 ± 0.9%, P  
ISSN:0363-6135
0002-9513
1522-1539
DOI:10.1152/ajpheart.1999.277.2.h660