High salt intake induce intracerebral hemorrhage and cerebral microvascular architecture changes in spontaneously hypertensive rats

戴志强; 张旋; 冯阳; 赵恒立; 左世伦; 刘昕; 冯华

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High salt intake induce intracerebral hemorrhage and cerebral microvascular architecture changes in spontaneously hypertensive rats

更新时间：2026-01-09

- High salt intake induce intracerebral hemorrhage and cerebral microvascular architecture changes in spontaneously hypertensive rats
- Journal of Army Medical University Vol. 38, Issue 21, Pages: 2291-2296(2016)
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  CLC： R544.1;R589.4;R743.34
- Published：2016
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戴志强,张旋,冯阳,赵恒立,左世伦,刘昕,冯华.高盐诱导自发性高血压大鼠脑出血及脑微血管构筑改变[J].陆军军医大学学报(原第三军医大学学报),2016,38(21):2291-2296.

　Dai Zhiqiang,Zhang Xuan,Feng Yang,Zhao Hengli,Zuo Shilun,Liu Xin,Feng Hua.High salt intake induce intracerebral hemorrhage and cerebral microvascular architecture changes in spontaneously hypertensive rats[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(21):2291-2296.
戴志强,张旋,冯阳,赵恒立,左世伦,刘昕,冯华.高盐诱导自发性高血压大鼠脑出血及脑微血管构筑改变[J].陆军军医大学学报(原第三军医大学学报),2016,38(21):2291-2296. DOI：

　Dai Zhiqiang,Zhang Xuan,Feng Yang,Zhao Hengli,Zuo Shilun,Liu Xin,Feng Hua.High salt intake induce intracerebral hemorrhage and cerebral microvascular architecture changes in spontaneously hypertensive rats[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(21):2291-2296. DOI：

摘要

目的探讨自发性高血压大鼠（spontaneously hypertensive rats，SHR）和正常血压大鼠（WistarKyoto rat，WKY）饲喂高盐饮食后脑出血特点及脑微血管结构改变。方法 6周龄雄性SHR和WKY大鼠各60只分别通过随机数字表分为两组，一组饲喂高盐饮食，一组饲喂常规饮食，每周测1次尾动脉收缩压，观察大鼠行为学改变、存活情况、神经功能缺损并评分，HE染色观察脑出血后血肿特点，干湿质量比法测定脑含水量，伊文氏蓝(Evans blue，EB)检测血脑屏障通透性，免疫荧光染色观察脑微血管改变，透射电镜观察脑微血管超微结构和紧密连接改变。结果与两组常规饮食大鼠相比，两组高盐饮食大鼠均出现血压升高、神经功能缺损症状，脑含水量和血脑屏障通透性增加，HE染色可见血管周围出现圆形渗出性出血，免疫荧光染色显示脑血管呈断续性改变，透射电镜可见脑血管与周围组织间隙增宽，紧密连接消失，管壁厚薄不均，出现空泡样改变。SHR所有改变较WKY显著（P0.01）。高盐饮食SHR 18周龄时全部死亡，高盐饮食WKY 19周龄时全部死亡，常规饮食大鼠均正常存活。结论高盐可单独引起大鼠血压升高、脑微血管结构改变，高血压可加重大鼠脑微血管损伤，两者可共同促进大鼠脑出血发生。

Abstract

Objective To investigate the characteristics of intracerebral hemorrhage and cerebral microvascular architecture changes in spontaneously hypertensive rats (SHR) and normotensive WistarKyoto rats (WKY) after high salt intake. Methods Sixty SHR rats and 60 WKY (male’ 6 weeks old) were randomly divided into 2 groups though the random number table. One group was fed with high salt diet

and the other with normal salt diet. Tail arterial systolic pressure was measured weekly

and behavioral changes and neurological deficit score were observed and evaluated everyday. HE staining was used to observe the hematoma characteristics

wet-dry weighing was used to detect cerebral water content

Evan’s blue staining was used to observe the permeability of blood brain barrier

immunofluorescence staining was performed to observe cerebral microvascular changes

and transmission electron microscopy was employed to observe cerebrovascular ultrastructure and tight connection changes after 8 weeks’ feeding. Results Compared with the 2 normal salt diet groups

high salt diet induced to increased blood pressure

neurological deficits

enhanced brain water content

and increased permeability of blood brain barrier. HE staining showed ring exudative hemorrhage around the blood vessels. Immunofluorescence staining displayed the discontinuous changes in cerebral microvessels. Transmission electron microscopy showed the widened gap between cerebral blood vessels and surrounding tissues

disappeared tight junctions

uneven thickness and vacuolar changes in the vascular wall. All of above changes were more significant in SHR rats than the WKY rats (P0.01). All of high salt SHR rats died at the age of 18 weeks

and the high salt WKY group died at the age of 19 weeks

but all of normal salt rats survived. Conclusion High salt diet induces blood pressure increase and cerebral microvascular structure changes

and hypertension aggravates cerebral microvascular injury in the rats. The 2 conditions can promote the occurrence of cerebral hemorrhage.

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