Figure 5.

Hearts of SA/SA mice showed differences in collagen and myocyte morphology. (A) Examples of variable and extensive collagen fibrosis in WT and SA/SA left ventricular myocardium. Panel A, WT+ANG II: Left ventricle. Collagen fibrosis appears as a focal region with increase in thickness of endomysium associated with adjacent cardiac myocytes. There appears to be minimal destruction or loss of myocytes associated with regions of fibrosis. Panel B, SA/SA+ANG II. Left ventricle. A typical large region of myocardial damage is characterized by extensive collagen fibrosis and loss and destruction of cardiac myocytes. In the central region of the fibrotic lesion, cardiac myocytes have been completely lost and undergoing destruction. The cardiac myocytes in the fibrotic lesion are reduced in size, but may still retain their nucleus (arrow c). Other cardiac myocytes associated with collagen lesion exhibit hypertrophied nuclei and condensed chromatin (arrow n). Scale Bar = 50 μm. (B) Changes in cardiac myocyte morphology. Trichrome stained sections of the left ventricles of WT and SA/SA mice treated with saline or ANG II were analyzed for loss of myofibrils and mass of myofibrils. Ventricles of SA/SA mice treated with ANG II showed significant loss of myofibrils compared to other groups (upper). Mass of the myofibrils was increased in WT, but decreased in SA/SA mice treated with ANG II (lower). Myofibrils of SA/SA mice exhibited a greater density than wild type mice. *P < 0.05; Kruskal-Wallis ANOVA followed by Dunn’s post hoc test.