Department of Obstetrics and Gynaecology, University Hospital Gasthuisberg, Katholieke Universiteit Leuven, Leuven, Belgium.
Placenta. 2010 Apr;31(4):320-6. doi: 10.1016/j.placenta.2010.01.011. Epub 2010 Feb 9.
As a follow-up to our previous study which revealed a surprisingly deeper endovascular trophoblast (ET) invasion on day 18 in a transgenic preeclamptic (PE) rat model (hAngiotensinogen female symbol x hRenin male symbol) compared to non-PE controls, we examined further changes in ET invasion and associated spiral artery (SA) remodelling at term (day 21). PE transgenic rats and non-PE reversely mated (RM) transgenic rats were compared to normal SD rats (C). Sections were stained to visualize trophoblast, fibrinoid, vascular smooth muscle (VSM) and endothelium. SA were evaluated in three depth levels in the mesometrial triangle (MT) using the KS-400 image analysis system. In separate transgenic rats, Doppler ultrasound was performed in uterine arteries, and the resistance indices (RI) were calculated. Although for the whole MT differences in ET invasion were no longer significant between the PE and C, indicating a partial catching up in C rats, there was still significantly more ET in the deepest level in the PE group as compared to the C and RM groups. At the same time the SA walls in PE rats contained significantly more fibrinoid (versus RM and C) and VSM (versus C). In all SA cross-sections, re-endothelialisation was prominent, but significantly different between PE and C group. The Doppler results showed a significantly lower RI in the arcuate uterine artery of the PE group compared to the C group. There was no evidence of elimination of deeply invaded ET at term, previously considered as a possible mechanism for restriction of vascular remodelling in human PE. The differences in vascular remodelling, previously described on day 18 by histology and Doppler data, were maintained on day 21, but there was extensive endothelial repair in the three groups. Atherosis-like lesions were observed in the three groups, most frequently in the RM group, but were never associated with placental infarcts.
作为我们之前研究的后续，该研究揭示了在血管内滋养细胞（ET）侵袭方面，转 Angiotensinogen 基因（hAngiotensinogen female symbol x hRenin male symbol）先兆子痫（PE）大鼠模型在第 18 天与非 PE 对照组相比有惊人的更深程度的侵袭，我们进一步检查了在足月（第 21 天）时 ET 侵袭和相关螺旋动脉（SA）重塑的变化。将 PE 转基因大鼠和非 PE 反转（RM）转基因大鼠与正常 SD 大鼠（C）进行比较。使用 KS-400 图像分析系统在中系膜三角（MT）的三个深度水平评估 SA。在单独的转基因大鼠中，进行了子宫动脉多普勒超声检查，并计算了阻力指数（RI）。尽管整个 MT 中 ET 侵袭的差异在 PE 和 C 之间不再显著，表明 C 大鼠有部分追赶，但在最深层的 ET 中 PE 组仍明显多于 C 和 RM 组。与此同时，PE 大鼠的 SA 壁含有明显更多的纤维蛋白样物质（与 RM 和 C 相比）和血管平滑肌（与 C 相比）。在所有 SA 横切面上，再内皮化很明显，但在 PE 和 C 组之间存在显著差异。多普勒结果显示，PE 组的弓形子宫动脉 RI 明显低于 C 组。在足月时，没有证据表明深层侵袭的 ET 被消除，这被认为是人类 PE 中血管重塑受限的一种可能机制。在第 18 天通过组织学和多普勒数据描述的血管重塑差异在第 21 天得以维持，但三组均有广泛的内皮修复。三组均观察到动脉粥样样病变，在 RM 组中最常见，但从未与胎盘梗死相关。
