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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Flow-induced vascular remodeling in the mesenteric artery of spontaneously hypertensive rats.
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Flow-induced vascular remodeling in the mesenteric artery of spontaneously hypertensive rats.

机译：自发性高血压大鼠肠系膜动脉血流诱导的血管重塑。

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摘要

The effect of an increased blood flow on vascular remodeling was studied in the mesenteric arteries of 11-12-week-old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto rats (WKY). Increased blood flow was induced by selective ligation of mesenteric arteries. Nearby arteries with normal blood flow were used as controls. 7-10 days after the ligation procedure, mesenteric arteries were fixed in situ at maximal relaxation by perfusion fixation. Morphometric measurement of vascular dimension was carried out with confocal microscopy. Apoptotic cells were detected by the TdT-mediated dUTP nick-end labelling method. Cell growth was quantified by using proliferating cell nuclear antigen (PCNA) in sections of paraffin-embedded vessels. In SHR, elevated blood flow increased the vessel wall dimension and the number of smooth muscle cell (SMC) layers and also increased the wall-to-lumen ratio and the number of PCNA-positive SMC, but did not change lumen size or number of apoptotic SMC.In WKY, on the other hand, increased blood flow resulted in an increase in lumen diameter, a reduction of apoptotic SMC, but no change in wall-to-lumen ratio, number of SMC layers, or number of PCNA-positive SMC. These results showed that mesenteric arteries from hypertensive and normotensive rats respond to an increase in blood flow differently: a lumen enlargement with reduced SMC apoptosis in WKY, but an increased wall-to-lumen ratio with enhanced SMC growth in SHR. Although it remains to be determined whether flow alteration is one of the initiating factors in the development of vascular remodeling in hypertension, we speculate that an increase in cardiac output, and therefore an increase in shear stress that occurs in young SHR, contributes to vascular remodelling in this model of hypertension.
机译：在11-12周大的自发性高血压大鼠（SHR）和年龄匹配的血压正常的Wistar-Kyoto大鼠（WKY）的肠系膜动脉中研究了增加的血流对血管重塑的影响。肠系膜动脉的选择性结扎引起血流量增加。使用正常血流的附近动脉作为对照。结扎手术后7-10天，通过灌注固定将肠系膜动脉原位固定在最大松弛处。用共聚焦显微镜进行血管尺寸的形态测量。通过TdT介导的dUTP切口末端标记法检测凋亡细胞。通过在石蜡包埋的血管切片中使用增殖细胞核抗原（PCNA）来定量细胞生长。在SHR中，升高的血流增加了血管壁的大小和平滑肌细胞（SMC）的层数，并增加了管腔比和PCNA阳性SMC的数目，但并未改变管腔的大小或数目。另一方面，在WKY中，血流量增加导致管腔直径增加，凋亡SMC减少，但壁腔比，SMC层数或PCNA阳性数没有变化。 SMC。这些结果表明，来自高血压和正常血压大鼠的肠系膜动脉对血流的增加反应不同：管腔增大，WKY的SMC凋亡减少，但管腔比增加，SHR的SMC增长增强。尽管尚需确定流量改变是否是高血压血管重塑发展的起始因素之一，但我们推测心输出量的增加以及因此在年轻SHR中发生的切应力的增加都有助于血管重塑在这种高血压模型中。

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