title: 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.
abstract: Scanning electron microscopy was used to compare the shape, size, and connection 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 myocytes 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 indices for SB, LB, and three selected types of cell junctions were measured in 100 cells from each heart and averaged for comparison studies. In the growing period (3-8 weeks of age), the LV myocytes were similar in shape and width in the two age-matched strains and grew similarly with the same L/W ratio. 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), the LB proliferated significantly, and the numbers of step-to-step and side-to-side junctions were diminished. In adult (15-35-week-old) WKY, LV cells continued to grow without much change in SB, LB, and the cell junctions, whereas in adult SHR, LV hypertrophy progressed with enhanced cardiomyocyte hypertrophy, increased number of SB, LB, and step-to-end junctions, and reduction 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, SB, LB, and cell junctions did not differ from those in adult WKY and SHR, except for LB thinning in the WKY and significant LB loss in the SHR. Age-related reductions 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 junctions which couple the cells for transverse conduction, and contribute to anisotropic discontinuous propagation and potential reentrant LV arrhythmias.
authors.affiliation: Department of Internal Medicine, Osaka Medical College, Takatsuki, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Okabe
authors.forename: K
authors.initials: K
authors.lastname: Kawamura
authors.forename: F
authors.initials: F
authors.lastname: Terasaki
authors.forename: T
authors.initials: T
authors.lastname: Hayashi
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D048429:Cell Size; D006352:Heart Ventricles / Q000648:ultrastructure*; D006973:Hypertension / Q000473:pathology*; D007365:Intercellular Junctions / Q000648:ultrastructure; D008297:Male; D008855:Microscopy, Electron, Scanning; D009206:Myocardium / Q000648:ultrastructure*; D009929:Organ Size; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D020257:Ventricular Remodeling