HYPERTROPHIC AND HYPERPLASTIC EFFECTS OF PREGNANCY ON THE RAT UTERINE ARTERIAL-WALL
HYPERTROPHIC AND HYPERPLASTIC EFFECTS OF PREGNANCY ON THE RAT UTERINE ARTERIAL-WALL
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DOI：
10.1016/0002-9378(94)90102-3
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发表时间：
1994-09-01
影响因子：
9.8
通讯作者：
OSOL, G
中科院分区：
文献类型：
--
作者：
CIPOLLA, M;OSOL, G
目的：本研究的目的是表征的细胞机制（肥大或增生）有助于子宫动脉growth during pregnancy.Study DESIGN：血管平滑肌细胞酶促分散从非妊娠（n = 4）和晚期妊娠（第20天至21日，n = 6）Sprague-Dawley大鼠的径向子宫动脉，并测量轴长。中孕给SD大鼠（第9 ~ 11天，n = 5）、晚期妊娠大鼠（n = 5）和非妊娠大鼠（n = 5）注射溴脱氧尿苷，免疫组化法观察子宫桡动脉和主动脉中分裂期和非分裂期血管平滑肌细胞和内皮细胞。从晚期妊娠血管中分离的血管平滑肌细胞比非妊娠动物长21%，从非妊娠大鼠的118 +/- 4 μ m增加到晚期妊娠大鼠的150 +/- 7 μ m。在非妊娠动物中，血管平滑肌细胞和内皮细胞的细胞增殖率都很低，但在妊娠期间，径向和主子宫动脉的细胞增殖率显着增加。然而，随着时间的推移，细胞分裂率的变化模式在不同的动脉段之间存在差异：在妊娠中期，血管平滑肌细胞和内皮细胞分裂率在较小的桡动脉中最高，而在足月时，子宫主动脉的有丝分裂指数值增加。子宫脉管系统的胚胎生长是通过动脉壁中细胞肥大和增生的组合来实现的。此外，在妊娠期间的不同时间在细胞分裂率的局部差异表明存在空间离散的血管网络内的生长机制。
OBJECTIVE: The purpose of this study was to characterize the cellular mechanisms (hypertrophy or hyperplasia) contributing to uterine arterial growth during pregnancy.STUDY DESIGN: Vascular smooth muscle cells were enzymatically dispersed from radial uterine arteries from nonpregnant (n = 4) and late pregnant (day 20 to 21, n = 6) Sprague-Dawley rats, and the axial length was measured. Midpregnant (days 9 to 11, n = 5), late pregnant (n = 5), and nonpregnant (n = 5) Sprague-Dawley rats were injected with bromodeoxyuridine, and immunohistochemistry was used to visualize dividing and nondividing vascular smooth muscle cells and endothelial cells in both radial and main uterine arteries.RESULTS: Vascular smooth muscle cells isolated from late-pregnant vessels were 21% longer than those from nonpregnant animals, increasing from 118 +/- 4 mu m in nonpregnant rats to 150 +/- 7 mu m in late-pregnant rats. Cell proliferation rates of both vascular smooth muscle cells and endothelial cells were quite low in nonpregnant animals but increased significantly during pregnancy in both radial and main uterine arteries. The pattern of changes in cell division rates over time, however, varied between the different arterial segments: in midpregnancy rates of both vascular smooth muscle cell and endothelial cell division were highest in the smaller radial arteries, whereas at term the mitotic index values were increased in main uterine arteries.CONCLUSIONS: Gestational growth of the uterine vasculature is accomplished by a combination of both cellular hypertrophy and hyperplasia in the arterial wall. Furthermore, local differences in cell division rates at different times during gestation suggest the existence of spatially discrete growth mechanisms within the vascular network.