Histologic and dynamic changes induced by chronic metabolic acidosis in the rat growth plate

Histologic and dynamic changes induced by chronic metabolic acidosis in the rat growth plate
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DOI:
10.1681/asn.v1261228
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发表时间:
2001-06-01
影响因子:
13.6
通讯作者:
Rodríguez, J
Rodríguez, J
中科院分区:
医学1区
文献类型:
--
作者:
Carbajo, E;López, JM;Rodríguez, J

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为了更好地了解持续性代谢性酸中毒导致生长发育障碍的病理生理学机制,本实验对经口灌胃氯化铵14d(AC)的幼年大鼠生长板的形态和动力学进行了观察,并与对照组(PF)配对饲养的非酸中毒大鼠(对照组[C])进行了比较。AC组(AC组,3.4±0.4;C组,8.4+/-0.6;PF组,6.4+/-0.5 mm(3)/d)每天新生骨体积(Mean+/-SEM)显著高于对照组(P<0.05)。AC组大鼠生长板高度(303.8+/-12.7um)低于C组(478.0+/-16.0um)和PF组(439.0+/-21.4um)。酸中毒对软骨细胞的增殖(用溴脱氧尿嘧啶核苷标记)和成熟(用软骨细胞大小、形状和每细胞基质体积的体视学评价)过程没有影响。与之相比,肥大软骨细胞的动力学发生了显著改变:每柱细胞的每日周转率(AC,4.4+/-0.4;C,8.0+/-0.8;PF,6.2+/-0.6)和软骨细胞的线推进速度(AC,5.7+/-0.5;C,11.2+/-0.9;PF,9.4+/-0.8微米/小时)均显著降低。这项研究显示了代谢性酸中毒对软骨细胞生长和软骨内骨形成的抑制作用。最后,数据显示,代谢性酸中毒导致生长板明显缩短,因为软骨细胞周转受到的影响比骨组织形成的影响更大。
To understand better the pathophysiology of growth impairment in persistent metabolic acidosis, the morphology and dynamics of the growth plate were studied in young rats grouped as follows: rats that were made acidotic by oral administration of ammonium chloride for 14 d (AC), nonacidotic rats that were fed ad libitum (control [C]), and nonacidotic rats that were pair-fed with the AC group (PF), AC rats became markedly acidotic and growth retarded. The volume of newly formed bone per day (mean +/- SEM) was significantly towered (P < 0.05) in AC rats (AC, 3.4 0.4; C, 8.4 +/- 0.6; PF, 6.4 +/- 0.5 mm(3)/d). Growth plate height was lower in AC rats (303.8 +/- 12.7 mum) than in either C (478.0 +/- 16.0 mum) or PF rats (439.0 +/- 21.4 mum). The processes of chondrocyte proliferation (assessed by bromodeoxyuridine labeling) and maturation (assessed by stereologic estimators of size and shape of chondrocytes and the volume of matrix per cell) were not impaired by acidosis. By contrast, the dynamics of hypertrophic chondrocytes were altered significantly: both cell turnover per column per day (AC, 4.4 +/- 0.4; C, 8.0 +/- 0.8; PF, 6.2 +/- 0.6) and linear velocity of advance of chondrocytes (AC, 5.7 +/- 0.5; C, 11.2 +/- 0.9; PF, 9.4 +/- 0.8 mum/h) were lowered si,gnificantly. The study presented here shows the inhibitory effect of metabolic acidosis an cartilage cell progression and endochondral bone formation. Finally, the data show that metabolic acidosis caused a marked shortening of the growth plate because chondrocyte turnover was affected to a greater extent than bone tissue formation.