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自发性高血压大鼠微血管模式改变对网络阻力的影响。

The effect of microvascular pattern alterations on network resistance in spontaneously hypertensive rats.

机构信息

Department of Biomedical Engineering, Tulane University, New Orleans, LA 70118, USA.

出版信息

Med Biol Eng Comput. 2012 Jun;50(6):585-93. doi: 10.1007/s11517-012-0912-x. Epub 2012 May 5.

Abstract

Structural microvascular rarefaction, defined by a loss of vessels, is a common characteristic of hypertension and has been associated with elevated microvascular resistance. However, determining the causal relationship between microvascular network structure and resistance requires a consideration of all pattern changes throughout a network. The objectives of this study were to determine whether microvascular rarefaction is associated with other network pattern alterations and to evaluate whether pattern alterations in hypertension necessarily contribute to increased microvascular resistance. Mesenteric tissues from age-matched (15-16 weeks) male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were harvested and immunolabeled for PECAM. SHR networks displayed a decreased microvascular area, arteriolar-venular (AV) length, number of AV branches, and number of capillary segments. In addition, SHR networks displayed increased AV connections per network compared to WKY networks. Based on network geometries, resistance per network was calculated using a computational model. For simulations with equal vessel diameter and with relative diameters based on reported intravital measurements, SHR microvascular network resistance was not elevated compared to the WKY level. Our results suggest that microvascular pattern alterations associated with hypertension are more complex than vessel loss, and that these combined alterations do not necessarily lead to elevated resistance.

摘要

结构微血管稀疏,即血管丧失,是高血压的一个常见特征,与升高的微血管阻力有关。然而,要确定微血管网络结构与阻力之间的因果关系,需要考虑网络中所有模式的变化。本研究的目的是确定微血管稀疏是否与其他网络模式改变有关,并评估高血压中的模式改变是否必然导致微血管阻力增加。从年龄匹配的(15-16 周)雄性自发性高血压大鼠(SHR)和正常血压的 Wistar-Kyoto(WKY)大鼠中采集肠系膜组织,并对 PECAM 进行免疫标记。SHR 网络显示出微血管面积、动静脉(AV)长度、AV 分支数量和毛细血管段数量减少。此外,与 WKY 网络相比,SHR 网络的 AV 连接数增加。根据网络几何形状,使用计算模型计算每个网络的阻力。对于具有相等血管直径的模拟以及基于报告的活体测量的相对直径,与 WKY 水平相比,SHR 微血管网络阻力并未升高。我们的结果表明,与高血压相关的微血管模式改变比血管丧失更为复杂,这些综合改变不一定导致阻力升高。

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