Remodeling of cardiomyocytes and their branches in juvenile, adult, and senescent spontaneously hypertensive rats and Wistar Kyoto rats: comparative morphometric analyses by scanning electron microscopy

Scanning electron microscopy was used to compare the shape, size, and conne ction of left ventricular (LV) myocytes between spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) at 3, 8, 15, 35, and 63 weeks of age . For either strain at each age, five rats were studied, in which LV mpocyt es consisted of a cylindrical trunk with series (SB) and/ or lateral branch (es) (LB) and step formations; cell junctions had 12 common basic patterns. The length (L), width (W), and L/W ratio of the myocytes, and various indi ces for SE, LB, and three selected types of cell junctions were measured in 100 cells from each heart and averaged for comparison studies. In the grow ing period (3-5 weeks of age), the LV myocytes were similar in shape and wi dth in the two age-matched strains and grew similarly with the same L/W rat io. In adolescent (15-week-old) WKY, LV cells grew with the same L/W ratio as in the younger rats, whereas in adolescent SHR, the cells showed a much greater increase in width than in length (disproportionate hypertrophy). th e LB proliferated significantly, and the numbers of step-to-step and side-t o-side junctions were diminished. In adult (15-35-week-old) WKY, LV cells c ontinued to grow without much change in SE, LB, and the cell junctions, whe reas in adult SHR, LV hypertrophy progressed with enhanced cardiomyocyte hy pertrophy, increased number of SE, LB, and step-to-end junctions, and reduc tion in the number of step-to-step and side-to-side junctions per cell. In aged (63 week-old) WKY and SHR, the indices of LV myocytes, SE. LB, and cel l junctions did not differ from those in adult WKY and SHR, except for LB t hinning in the WKY and significant LB loss in the SHR. Age-related reductio ns in side-to-side- and step-to-step junctions, and LB loss with myocardial fibrosis in adult and aged SHR may indicate increased loss of gap junction s which couple the cells for transverse conduction, and contribute to aniso tropic discontinuous propagation and potential reentrant LV arrhythmias.