Lei L Q, Rubin S A, Fishbein M C
Division of Anatomical Pathology, Cedars-Sinai Medical Center, Los Angeles, California.
Lab Invest. 1988 Sep;59(3):357-62.
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.
我们已经证明，过量的生长激素（GH）会导致大鼠左心室肥厚。为了进一步描述该模型的细胞生长情况，我们对6只对照（C）大鼠和5只GH刺激大鼠的灌注固定左心室（LV）的5微米和1微米切片进行了光镜和电镜形态计量学联合研究。经过几周的GH刺激后，大鼠的全心重量、左心室重量和右心室重量分别增加了45%、46%和43%。然而，两组之间左心室与体重的比值以及右心室与体重的比值均无显著差异。由于每个面积的细胞核数量减少（819±80对718±52/mm²，p<0.05）且细胞核长度增加（16.9±1.7对19.7±0.5微米，p<0.01），GH组的细胞核/体积减少了25%。由于GH组和C组的心肌细胞体积分数相同，每个细胞核的心肌细胞体积增加（C组为16.5±1.9，GH组为20.8±1.1×10³微米³，p<0.01）。由于心肌细胞的横截面积没有变化（C组为242±26对GH组为244±23微米²，p>0.50），每个细胞核的细胞长度增加了26%（C组为68.5±8.6对GH组为86.0±7.8微米，p<0.01）。与C组相比，GH组左心室壁中部的平均面积增加了35%（p<0.01），但随着左心室腔半径增加（C组为1.85±0.5对GH组为2.50±0.6毫米，p = 0.06），室壁厚度未改变（C组为2.1±0.4对GH组为2.2±0.2毫米，p>0.20）。随着GH组左心室舒张末压降低，收缩期周向壁应力未改变（C组为55.3±21.1对GH组为57.2±22.5×10³达因/厘米²，p>0.50）。我们得出结论，该模型的左心室肥厚与腔扩张和心肌细胞长度增加有关；这种适应性反应倾向于将容量负荷增加对壁应力的影响降至最低。
