Cited 3 times since 1989 (0.1 per year) source: EuropePMC Cardiovascular research, Volume 23, Issue 4, 1 1 1989, Pages 308-314 Comparison of myocardial changes between pressure induced hypertrophy and normal growth in the rat heart. van der Laarse A, Vliegen HW, van der Nat KH, Hollaar L, Egas JM, Swier GP, van den Broek AJ

To evaluate differences in tissue composition between hearts with pressure overload hypertrophy and normal hearts of comparable weight, 30 rat hearts with aortic constriction of 4, 10 and 30 days, and nine hearts of sham operated controls were studied. Surgery was performed at age 70 days. Morphometric analysis of myocardial tissue sections revealed (1) myocyte hypertrophy in left ventricular myocardium of hypertrophic hearts was proportional to heart weight, and in normal growth myocyte volume increased in proportion to heart weight; (2) myocyte number in left ventricular myocardium was identical in hypertrophic and normal hearts; (3) non-muscle cell proliferation was proportional to heart weight identically in hypertrophic and normal hearts; (4) volume fractions of myocytes were significantly lower in hypertrophic hearts [0.76(SD 0.05)] than in normal hearts [0.82(0.04)]; (5) volume fractions of all nuclei, myocyte nuclei and non-myocyte nuclei were similar in hypertrophic and normal hearts; (6) measured ventricular DNA content increased with heart weight identically in hypertrophic and normal hearts, and equalled DNA content calculated using the data on tissue composition. Neither right ventricular weight nor right ventricular DNA content were affected by the presence of left ventricular hypertrophy. We conclude that left ventricular hypertrophy due to aortic constriction in the rat resulted in changes of myocardial tissue composition similar to the changes associated with normal growth. Tissue composition of hypertrophic rat hearts corresponds strikingly to that of normal rat hearts with comparable heart weight, although myocardial changes in hypertrophy develop considerably faster than in normal growth.

Cardiovasc Res. 1989 4;23(4):308-314