Connexin43 as a determinant of myocardial infarct size following coronary occlusion in mice
Shigeto Kanno, MD, PhD*,
Attila Kovacs, MD*,
Kathryn A. Yamada, PhD* and
Jeffrey E. Saffitz, MD, PhD, FACC*,*
* Departments of Surgery, Medicine, and Pathology, and the Center for Cardiovascular Research, Washington University School of Medicine, St. Louis, Missouri, USA
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Figure 1 Representative trichrome-stained sections of mouse myocardial infarcts. (Left) A typical anteroapical infarct (arrow) observed eight days after MI surgery. (Center) Edematous, highly cellular granulation tissue with residual necrotic muscle (arrow) in a healing infarct (bar = 50 µm). (Right) Mature, sparsely cellular scar tissue in a fully healed infarct (bar = 100 µm).
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Figure 2 Changes in left ventricular end-diastolic volume (LVVd) (A) and left ventricular (LV) mass (B) between days 1 and 7 after myocardial infarction and LV ejection fraction on day 7 (C) as a function of infarct size measured echocardiographically in Cx43+/– (solid circles) and Cx43+/+ (open circles) mice.
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Figure 3 Left ventricular (LV) end-diastolic volume (A) and ejection fraction (B) as a function of infarct size measured one week (triangles) and 10 weeks (squares) after myocardial infarction (MI) in Cx43+/– (solid symbols) and Cx43+/+ (open symbols) mice.
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Figure 4 Infarct size measured histologically 8 days and 10 weeks after left anterior descending coronary artery occlusion in Cx43+/– and Cx43+/+ mice. LV = left ventricular; MI = myocardial infarction. *p = 0.037.
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