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Am J Physiol Heart Circ Physiol 282: H2152-H2158, 2002. First published January 24, 2002; doi:10.1152/ajpheart.00777.2001
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Vol. 282, Issue 6, H2152-H2158, June 2002

Cardiac mast cell-mediated activation of gelatinase and alteration of ventricular diastolic function

Amanda L. Chancey, Gregory L. Brower, and Joseph S. Janicki

Department of Anatomy, Physiology, and Pharmacology, Auburn University, Auburn, Alabama 36849

Mast cells contain proteases capable of activating matrix metalloproteinases (MMPs). However, given the relatively low density of mast cells in the myocardium (i.e., 1.5-5.3 cells/mm2), it is unknown whether these enzymes are present in sufficient quantities in the normal heart to mediate MMP activation. Accordingly, this study sought to determine whether chemically induced degranulation of cardiac mast cells (with compound 48/80) would have an effect in isolated, blood-perfused, functioning rat hearts. Mast cell degranulation produced a 15% increase in histamine levels present in the coronary efflux, a significant increase in myocardial water (i.e., edema) relative to normal values (80.1 ± 3.4% vs. 77.4 ± 1.08%, P <=  0.03), a substantial activation of MMP-2 (126% increase relative to controls, P <=  0.02), and a marked decrease in myocardial collagen volume fraction (0.46 ± 0.10% vs. 0.97 ± 0.33%, P <=  0.001). Furthermore, although an increase in ventricular stiffness was expected due to the extent of edema resulting from mast cell degranulation, modest ventricular dilatation was observed. These findings clearly demonstrate that the number of mast cells present in normal hearts is sufficient to mediate activation of MMPs and produce extracellular matrix degradation, thereby potentially causing subsequent ventricular dilatation.

compound 48/80; isolated heart; coronary flow; histamine; collagen volume fraction; pressure-volume relationship; matrix metalloproteinase


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