Physiological and immunocytochemical evidence for a new concept of blood flow regulation in the corpus luteum.
Physiological and immunocytochemical evidence for a new concept of blood flow regulation in the corpus luteum.
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黄体血流调节新概念的生理学和免疫细胞化学证据。
DOI：
10.1095/biolreprod42.1.139
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发表时间：
1990
影响因子：
3.6
通讯作者：
Keyes,PL
中科院分区：
文献类型：
--
作者：
Wiltbank,MC;Gallagher,KP;Christensen,AK;Brabec,RK;Keyes,PL
为了解释黄体中的高血流速率，我们假设黄体血管提供最小的流动阻力并且不能进行血管运动。通过在三个动脉血压水平下用示踪剂标记的微球测量黄体和卵巢基质中的血流量，在假孕中期的兔子中测试了这一假设，通过收缩卵巢动脉上方的主动脉来操纵。此外，还用形态学和免疫细胞化学技术观察了卵巢血管平滑肌的分布。动脉压的降低被黄体血流量的减少所抵消，而卵巢间质血流量不变。与我们的假设相一致，在Lectin体中血管提供的低水平血管阻力没有变化，支持它们最大扩张且不能自动调节的观点。形态学上，黄体内的血管表现为无平滑肌的大窦状毛细血管，为生理学上缺乏血管控制提供了解剖学解释。使用针对肌肉特异性中间丝结蛋白的抗体，用免疫细胞化学证实血管平滑肌的缺失。荧光素标记的抗体在卵巢间质内和黄体被膜附近的动脉和小动脉上有明显的装饰，而在假孕黄体内没有血管的装饰，这进一步证明了黄体内的血管缺乏改变血管口径所必需的平滑肌。根据这些发现，我们提出了一个新的方案来解释卵巢内血流调节。与大多数组织一样，卵巢间质的血管阻力受组织内小动脉扩张或收缩的剧烈调节。相反，黄体内的血管阻力被建模为相对不稳定的参数，由黄体血管系统的形态学特征在低水平上改变。因此，黄体在线性（最大“血管舒张”）压力-流量曲线上运行，不主动调节组织内血流，并且仅通过黄体外血管的变化进行灌注的急性调节。
To explain the high rate of blood flow in the corpus luteum, we hypothesize that luteai blood vessels offer minimal resistance to flow and are incapable of vasomotion. This hypothesis was tested in rabbits at mid-pseudopregnancy by measuring blood flow in the corpus luteum and ovarian stroma with tracer-labeled micro-spheres at three levels of arterial blood pressure, which was manipulated by constricting the aorta above the ovarian artery. In addition, the distribution of vascular smooth muscle in the ovary was evaluated with morphological and immunocytochemical techniques. Decreases in arterial pressure were paralleled by reductions in bloodflow in the corpus lutewn, whereas ovarian stromal bloodflow was unchanged. Consistent with our hypothesis, there was no change in the low level of vascular resistance offered by blood vessels in the corpus luseum, supporting the view that they are maxinally dilated and incapable of autoregulation. Morphologically, the vessels within the corpus luteum appeared as large sinusoidal capillaries without smooth muscle, providing an anatomical explanation for the lack of vasomotor control demonstrated physiologically. The absence of vascular smooth muscle was confirmed with immunocytochemistry using an antibody against the muscle-specific intermediate filament, desmin. The fluorescein-labeled antibody decorated arteries and arterioles within the ovarian stroma and near the capsule of the corpus luteum, bus did not decorate vessels in the corpus luteum ofpseudopregnancy, providing additional evidence that the vessels of the corpus liaeum lack the smooth muscle investment necessary to change vascular caliber. From these findings, we have proposed a novel scheme to explain intraovarian blood flow regulation. Vascular resistance in the ovarian stroma, as in most tissues, is acutely regulated by dilation or constriction of intratissue arterioles. In contrast, vascular resistance within the corpus luteum is modeled as a relatively invari able parameter, flxed at a low level by the morphological characteristics of the luteal vasculature. Therefore, the corpus luteum operates on a linear(maximally“vasodilated”) pressure-flow curve, does not actively regulate intratissue blood flow, and is subject to acute regulation of perfusion only through changes in extra-luteal vessels.