MECHANICS OF CEREBRAL ARTERIOLES IN HYPERTENSIVE RATS
MECHANICS OF CEREBRAL ARTERIOLES IN HYPERTENSIVE RATS
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DOI：
10.1161/01.res.62.1.56
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发表时间：
1988-01-01
影响因子：
20.1
通讯作者：
HEISTAD, DD
中科院分区：
文献类型：
--
作者：
BAUMBACH, GL;DOBRIN, PB;HEISTAD, DD
慢性高血压与脑血管肥大有关。以往对慢性高血压患者脑血管力学特性的研究主要针对大的脑动脉。本研究的目的是首先开发一种方法来检查在体内的脑小动脉的血管力学和第二，以确定是否存在慢性高血压的脑小动脉的刚度改变。我们通过测量软脑膜小动脉压力、内径和壁厚，计算了年龄匹配、麻醉的易卒中自发性高血压大鼠（SHRSP）和Wistar京都大鼠（WKY）软脑膜小动脉的周向应力和应变。用servonull系统测量软脑膜小动脉压。软脑膜小动脉平滑肌用乙二胺四乙酸（EDTA）灭活，并在逐步减压过程中检查压力-直径关系。在3- 4月龄大鼠的平滑肌失活之前，SHRSP中的软脑膜小动脉压力比WKY中的大（110 . ±. 4对75 +-。2 mm Hg [平均值±。SE]; p < 0.05）。在软脑膜小动脉压力的主要水平下测量的软脑膜小动脉直径在SHRSP中小于WKY（52 ± 0.05）。5对63 +-。3 μ m; p < 0.05）。在平滑肌失活后，两组中软脑膜小动脉压力为70 mm Hg时软脑膜小动脉的直径相似：104 ± 0.5mm Hg。SHRSP中为6 μ m，而SHRSP中为109 . ±. 3 μ m（p > 0.05）。壁厚为4.5 ±。0.2在SHRSP中为4.1 μ m，在SHRSP中为4.1 μ m。0.1在WKY中的μ m（p > 0.05）。失活的SHRSP软脑膜微动脉的应力-应变关系右移，表明年轻SHRSP软脑膜微动脉的周向刚度降低。为了确定软脑膜小动脉肥大是否与小动脉硬度增加有关，我们研究了6至8个月大的SHRSP和WKY的应力-应变特性。在老年大鼠中，活动和失活的软脑膜小动脉的直径SHRSP小于WKY。SHRSP的室壁厚度显著大于WKY（5.8 ± 0.01）。0.5与3.8 .+-相比。0.2μ m; p < 0.05）。而6 ~ 8月龄SHRSP的应力-应变关系较WKY更右移。我们的结论是，尽管有明显的血管肥大，但SHRSP的脑小动脉硬度降低。
Chronic hypertension is associated with hypertrophy of cerebral blood vessels. Previous studies of the mechanical properties of cerebral vessels in chronic hypertension have examined large cerebral arteries. The goals of this study were first to develop a method to examine vascular mechanics of cerebral arterioles in vivo and second to determine whether the stiffness of cerebral arterioles is altered in the presence of chronic hypertension. We calculated circumferential stress and strain of pial arterioles in age-matched, anesthetized stroke-prone spontaneously hypertensive rats (SHRSP) and in Wistar Kyoto rats (WKY) from measurements of pial arteriolar pressure, inner diameter, and wall thickness. Pial arteriolar pressure was measured with a servonull system. Smooth muscle of pial arterioles was deactivated with ethylenediaminetetraacetic acid (EDTA), and pressure-diameter relations were examined during step-wise reductions in pressure. Prior to deactivation of smooth muscle in 3- to 4-month-old rats, pial arteriolar pressure was greater in SHRSP than in WKY (110 .+-. 4 versus 75 .+-. 2 mm Hg [mean .+-. SE]; p < 0.05). Pial arteriolar diameter, which was measured at prevailing levels of pial arteriolar pressure, was less in SHRSP than in WKY (52 .+-. 5 versus 63 .+-. 3 .mu.m; p < 0.05). Following deactivation of smooth muscle, diameter of pial arterioles at 70 mm Hg of pial arteriolar pressure was similar in the two groups: 104 .+-. 6 .mu.m in SHRSP and 109 .+-. 3 .mu.m in WKY (p > 0.05). Wall thickness was 4.5 .+-. 0.2 .mu.m in SHRSP and 4.1 .+-. 0.1 .mu.m in WKY (p > 0.05). The stress-strain relation in deactivated pial arterioles was shifted to the right in SHRSP, which indicates that circumferential stiffness of pial arterioles is decreased in young SHRSP. To determine whether hypertrophy of pial arterioles, which occurs with maturation, is associated with increases in arteriolar stiffness, we examined stress-strain characteristics in 6- to 8-month-old SHRSP and WKY. In older rats, diameter of both active and deactivated pial arterioles was less in SHRSP than in WKY. Wall thickness was significantly greater in SHRSP than in WKY (5.8 .+-. 0.5 versus 3.8 .+-. 0.2 .mu.m; p < 0.05). The stress-strain relation, however, was shifted even further to the right in 6- to 8-month-old SHRSP with respect to WKY. We conclude that the stiffness of cerebral arterioles is decreased in SHRSP with established hypertension despite pronounced vascular hypertrophy.