Abstract

Perimenopausal women have a higher risk of mortality within 2 years of myocardial infarction than similarly aged men despite having less left ventricular dysfunction. Cardiac mast cells (CMC) contribute to inflammation after I/R injury. Recent work suggests that estrogen stimulates mast cell degranulation. We tested whether I/R produced increases in CMC numbers and whether degranulation was more extensive 8 weeks after I/R in male or female rats. The number of stable or degranulating CMCs was determined in regions high in CMC density. Three regions were studied: 1) the ventral epicardial surface at the base of the superior vena cava, 2) the rostral pole of the left atrium and 3) the dorsal surface surrounding the right and left pulmonary veins. Both males (P<0.001) and females (P<0.05) showed reductions in fractional shortening (FS) after I/R compared to controls, while males had lower FS after I/R than females (19.3 ± 2.5 vs. 33.3 ± 3.4%, P<0.01). Left ventricular end‐diastolic diameter was increased after I/R only in males (0.77± 0.08 vs. 0.99 ± 0.04, P<0.01). Numbers of CMCs of either sex was not different 8 weeks after I/R in any region examined. The number of degranulating CMCs and the percent of total CMCs that were degranulating were increased in region 3 after I/R in both sexes (26.8 vs. 77.8% in males, P<0.001; and 25.8 vs. 72.3% in females, P<0.001). The percentage of degranulating CMCs was increased similarly across sex in regions 1 and 2 (45‐59% vs. 23‐29%, P<0.05). The data indicate that CMC degranulation continues 8 weeks after I/R injury in regions rostral to the original ischemia. This effect is similar in male and female rats despite less I/R‐induced left ventricular dysfunction in females.

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