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首页> 外文期刊>American Journal of Physiology >Cardiac mast cell-mediated activation of gelatinase and alteration of ventricular diastolic function.
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Cardiac mast cell-mediated activation of gelatinase and alteration of ventricular diastolic function.

机译：心脏肥大细胞介导的明胶酶激活和心室舒张功能的改变。

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摘要

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/mm(2)), 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 < or = 0.03), a substantial activation of MMP-2 (126% increase relative to controls, P < or = 0.02), and a marked decrease in myocardial collagen volume fraction (0.46 +/- 0.10% vs. 0.97 +/- 0.33%, P < or = 0.001). Furthermore, although an increase in ventricular stiffness was expecteddue 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.
机译：肥大细胞包含能够激活基质金属蛋白酶（MMP）的蛋白酶。然而，鉴于心肌中肥大细胞的密度相对较低（即1.5-5.3个细胞/ mm（2）），尚不清楚这些酶是否在正常心脏中以足够的量存在以介导MMP激活。因此，本研究试图确定化学诱导的心肌肥大细胞脱粒（使用化合物48/80）是否会对分离的，血液灌注的，正常运作的大鼠心脏产生影响。肥大细胞脱颗粒使冠状外排中存在的组胺水平增加15％，相对于正常值（80.1 +/- 3.4％与77.4 +/- 1.08％，P <或= 0.03），MMP-2的大量激活（相对于对照组增加126％，P <或= 0.02）以及心肌胶原蛋白体积分数的明显减少（0.46 +/- 0.10％对0.97 +/- 0.33 ％，P <或= 0.001）。此外，尽管由于肥大细胞脱粒引起的水肿程度，预计室性刚度会增加，但是观察到适度的室性扩张。这些发现清楚地表明，正常心脏中存在的肥大细胞数量足以介导MMP激活并产生细胞外基质降解，从而潜在地引起随后的心室扩张。

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