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Updated: Feb 16, 2026

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
Published on: April 30, 2020
Structural compensatory mechanisms in rat heart in early spontaneous hypertension
Abstract:
The response of the left ventricle (LV) during the development of spontaneous hypertension (SH) in rats was studied morphometrically at 21, 28, 35, and 45 days after birth and compared with that of normotensive (WK) controls. LV hypertrophy, varying from 24 to 27%, was characterized by the preservation of the volume fraction of capillary lumen and capillary luminal surface in the myocardium, as a result of capillary proliferation. From 21 to 45 days the number of capillaries per unit area of myocardium increased 68% in SH rats by the insertion in parallel of new capillary elements among the myocytes. This estimation was obtained by correcting the value of capillary density at 45 days for the amount of spreading produced by myocyte growth during this interval. On a similar basis capillary proliferation was only 24% in WK rats. Myocyte growth in experimental animals (151%) was achieved by a 77% enlargement in myocyte cross-sectional area (MCSA) and by a 42% lengthening of the cells. In controls myocyte expansion (124%) was the result of comparable increments in MCSA (47%) and myocyte length (53%).
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