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1 Cardiology Section, Department of Veterans Affairs Medical Center and Division of Cardiology, University of Colorado Health Sciences Center, Denver, Colorado 80220; 2 Departments of Medicine and 3 Biochemistry and Molecular Biology, University of Miami School of Medicine, Miami, Florida 33101; and 4 Department of Pathology and 5 Cardiovascular Research Institute, University of California, San Francisco, California 94143
Severe ischemic
injury or infarction of myocardium may cause activation of matrix
metalloproteinases (MMPs) and damage the interstitial matrix. However,
it is unknown whether MMP activation and matrix damage occur after
moderate ischemia and reperfusion that result in myocardial stunning
without infarction, and if so whether such changes contribute to
postischemic myocardial expansion and contractile dysfunction. To
address these questions, open-chest anesthetized pigs underwent 90 min
of regional ischemia (subendocardial blood flow 0.4 ± 0.1 ml
· g
1 · min1) and 90 min of
reperfusion. After ischemia plus reperfusion, histological and
ultrastructural examination revealed no myocardial infarction or
inflammatory cell infiltration. Myocardial MMP-9 content increased
threefold with a fourfold increase in the active form
(P < 0.001). Myocardial collagenase content doubled
(P < 0.01) but remained in latent form. MMP-2 and
tissue inhibitors of metalloproteinases were unaffected. Despite
increases in MMPs, collagen ultrastructure (assessed by cell maceration
scanning electron microscopy) was unaltered. Intracoronary
administration of the MMP inhibitor GM-2487 did not prevent or
attenuate myocardial expansion (assessed by regional diastolic
dimensions at near-zero left ventricular pressure) or contractile
dysfunction. We conclude that although moderate ischemia and
reperfusion alter myocardial MMP content and activity, these effects do
not result in damage to interstitial collagen, nor do they contribute
to myocardial expansion or contractile dysfunction.
ventricular function; collagenase; gelatinase; scanning electron microscopy; enzyme inhibitors
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