title: Cardiac architectural changes with hypertrophy induced by excess growth hormone in rats.
abstract: We have shown that excess growth hormone (GH) causes left ventricular hypertrophy in rats. To further characterize cell growth of this model, combined light and electron microscopic morphometric studies were done on 5- and 1-micron sections of the perfusion fixed left ventricle (LV) in 6 control (C) and 5 GH-stimulated rats. Total ventricular weight, LV weight and right ventricle weight were increased 45, 46, and 43%, respectively, in the rats after a few weeks of GH stimulation. However, neither the ratio of LV to body weight, nor right ventricle to body weight were significantly different between the two groups. Nuclei (n)/volume decreased by 25% in GH due to a decreased number of n/area (819 +/- 80 versus 718 +/- 52/mm2, p less than 0.05) and an increased n length (16.9 +/- 1.7 versus 19.7 +/- 0.5 micron, p less than 0.01). As the volume fraction of myocytes was the same in GH and C, the volume of myocytes/n increased (16.5 +/- 1.9 in C to 20.8 +/- 1.1 x 10(3) micron3 in GH, p less than 0.01). Since no change was found in cross-sectional area of myocytes (242 +/- 26 in C versus 244 +/- 23 micron2 in GH, p greater than 0.50) cell length/nucleus increased by 26% (68.5 +/- 8.6 in C versus 86.0 +/- 7.8 micron in GH, p less than 0.01). The average area of mid-LV wall increased by 35% in GH compared with C (p less than 0.01), but wall thickness was unchanged (2.1 +/- 0.4 in C versus 2.2 +/- 0.2 mm in GH, p greater than 0.20) as LV cavity radius increased (1.85 +/- 0.5 in C to 2.50 +/- 0.6 mm in GH, p = 0.06). With decreased developed pressure of LV in GH, systolic circumferential wall stress was unchanged (55.3 +/- 21.1 in C versus 57.2 +/- 22.5 x 10(3) dyne/cm2 in GH, p greater than 0.50). We conclude that left ventricular hypertrophy of this model is associated with cavity dilation and increased myocyte cell length; this adaptive response tends to minimize the effects of increased volume load on wall stress.
authors.affiliation: Division of Anatomical Pathology, Cedars-Sinai Medical Center, Los Angeles, California.
authors.forename: L Q
authors.initials: LQ
authors.lastname: Lei
authors.forename: S A
authors.initials: SA
authors.lastname: Rubin
authors.forename: M C
authors.initials: MC
authors.lastname: Fishbein
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D002196:Capillaries / Q000502:physiology; D006332:Cardiomegaly / Q000139:chemically induced / Q000473:pathology*; D003326:Coronary Circulation; D005260:Female; D013006:Growth Hormone / Q000494:pharmacology*; D006352:Heart Ventricles; D009206:Myocardium / Q000473:pathology*; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D011920:Rats, Inbred WF; D013314:Stress, Mechanical
chemical_list: D013006:Growth Hormone