Fig. 3
Masson’s trichrome staining of ventricles in rats with CHF 10 weeks after treatment. a Representative biventricular sections of RMI. The region surrounded by a green line showed area at risk. Scale bars, 2 mm. b Representative images of cardiac fibrosis in the noninfarcted area. c Representative myocyte cross sections (papillary cardiomyocytes). Scale bars, 50 μm. d Area at risk (UT, 38 ± 5%, n = 12; DT, 38 ± 6%, n = 15; MT, 38 ± 4%, n = 18; DMT, 39 ± 5%, n = 14). e Infarct size (infarcted area/area at risk) (UT, 51 ± 2%, n = 12; DT, 33 ± 3%, n = 15; MT, 56 ± 3%, n = 18; DMT, 35 ± 3%, n = 14). f Cardiac fibrosis index in the noninfarcted regions (UT, 5.0 ± 0.6%/field, n = 10, 60 fields of view; DT, 2.7 ± 0.2%/field, n = 14, 84 fields; MT, 4.9 ± 0.3%/field, n = 18, 108 fields; DMT, 2.4 ± 0.2%/field, n = 14, 84 fields). g Myocyte cross-sectional area in the noninfarcted region (UT, 1118 ± 98 μm2/cell, n = 7, 312 cells; DT, 683 ± 34 μm2/cell, n = 12, 668 cells; MT, 1218 ± 123 μm2/cell, n = 7, 264 cells; DMT, 465 ± 33 μm2/cell, n = 6, 869 cells). h Representative micrographs of blood microvessels (von Willebrand factor [vWF, red]) immunostaining in the peri-infarct and noninfarcted (septum) regions in rats with CHF. Scale bars, 50 μm. Quantitative analysis of microvessel density in (i) peri-infarct region (UT, 64 ± 10/field, n = 6, 21 fields of view; DT, 119 ± 11/field, n = 6, 21 fields; MT, 52 ± 7/field, n = 6, 22 fields; DMT, 103 ± 8/field, n = 7, 36 fields); (j) in the septum (UT, 44 ± 8/field, n = 6, 16 fields; DT, 105 ± 18/ field, n = 6, 11 fields; MT, 62 ± 20/field, n = 6, 16 fields; DMT, 82 ± 8/field, n = 7, 22 fields). Values are expressed as means ± SEMs. Data are shown as box-and-whisker plots for area at risk, MI size, cardiac fibrosis, myocyte cross-sectional area, and microvessels in all animals. *P < 0.05, **P < 0.01 vs. UT; ††P < 0.01 vs. MT, using nonparametric Kruskal–Wallis tests, followed by Dunn’s tests