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局部子宫胎盘因素在大鼠妊娠期间负责诱导子宫动脉肌源性张力。

Local uteroplacental influences are responsible for the induction of uterine artery myogenic tone during rat pregnancy.

作者信息

Gokina Natalia I, Kuzina Olga Y, Fuller Robert, Osol George

机构信息

Department of Obstetrics, Gynecology and Reproductive Sciences, College of Medicine, University of Vermont, Burlington, Vermont 05405, USA.

出版信息

Reprod Sci. 2009 Nov;16(11):1072-81. doi: 10.1177/1933719109340927. Epub 2009 Aug 5.

Abstract

Uterine artery constrictor responses to elevation of intraluminal pressure (myogenic tone) are considerably enhanced in late pregnant rats, although the underlying causes remain unknown. A single uterine horn ligation model was used to differentiate local from systemic influences, and to test the hypothesis that factors associated with the site of placentation, rather than systemic hormonal changes, are primarily involved in the induction of this adaptive process. Radial uterine arteries were dissected from the gravid and nongravid uterine horns of late pregnant rats, cannulated, and pressurized. Changes in arterial diameter and smooth muscle Ca(2+) in response to the elevation of intraluminal pressure were studied using intact and endothelium-denuded arteries loaded with the ratiometric Ca(2+)-sensitive dye fura-2. Elevations of pressure from 10 to 60 and 100 mm Hg resulted in passive arterial distention of arteries from nongravid horns with a minor change in Ca(2+). In contrast, arteries from gravid horns developed myogenic tone associated with a significant elevation in Ca(2+). Synchronous oscillations in Ca(2+) and lumen diameter were frequently observed in vessels from gravid horns. Endothelial denudation augmented tone in the gravid horn but did not uncover myogenic tone in vessels from the nongravid horn. In summary, pregnancy-associated uterine artery myogenic behavior is due to an upregulation of calcium-handling mechanisms, occurs independently of the endothelium, and is induced by local uteroplacental influences.

摘要

在妊娠晚期大鼠中,子宫动脉对管腔内压力升高(肌源性张力)的收缩反应显著增强,但其潜在原因尚不清楚。采用单侧子宫角结扎模型来区分局部和全身的影响,并检验以下假设:与胎盘着床部位相关的因素而非全身激素变化,是诱导这一适应性过程的主要原因。从妊娠晚期大鼠的妊娠子宫角和非妊娠子宫角中分离出子宫径向动脉,插管并加压。使用装载了比率型钙敏感染料fura-2的完整动脉和内皮剥脱动脉,研究管腔内压力升高时动脉直径和平滑肌Ca(2+)的变化。压力从10毫米汞柱升高到60毫米汞柱和100毫米汞柱时,非妊娠子宫角的动脉出现被动扩张,Ca(2+)仅有轻微变化。相比之下,妊娠子宫角的动脉产生了与Ca(2+)显著升高相关的肌源性张力。妊娠子宫角血管中经常观察到Ca(2+)和管腔直径的同步振荡。内皮剥脱增强了妊娠子宫角的张力,但未揭示非妊娠子宫角血管的肌源性张力。总之,妊娠相关的子宫动脉肌源性行为是由于钙处理机制上调所致,独立于内皮发生,并由局部子宫胎盘影响所诱导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9934/2759862/43a580181627/nihms145125f1.jpg

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