Calcification of medial elastic fibers and aortic elasticity
Calcification of medial elastic fibers and aortic elasticity
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DOI：
10.1161/01.hyp.29.4.999
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发表时间：
1997-04-01
期刊：
影响因子：
8.3
通讯作者：
Atkinson, J
中科院分区：
文献类型：
--
作者：
Niederhoffer, N;LartaudIdjouadiene, I;Atkinson, J
我们检验了这样一个假设，即壁成分的简单变化（弹性纤维的中膜钙超载）可以降低主动脉弹性。高维生素D加尼古丁（VDN）可引起幼鼠钙超载。两个月后，在未麻醉的，不受约束的大鼠的中央主动脉平均血压的测量显示，VDN大鼠患有孤立的收缩期高血压，但平均血压是正常的。原位加压固定后测定的壁厚和内径不变，计算的壁应力也不变。根据（1）弹性模量（采用Moens-Korteweg方程和未麻醉、未受限制大鼠和动脉尺寸中的主动脉脉搏波速度值确定）和（2）等压弹性（=苯肾上腺素输注、去髓大鼠制备物中脉搏波速度与平均管腔内压力相关的斜率）估计壁刚度。两者都增加后VDN，都显着相关的壁钙含量和弹性蛋白特异性氨基酸锁链素和异锁链素。VDN模型出现左心室肥厚，左心室质量与其等压弹性有关。总之，弹性蛋白钙质沉着症引起弹性纤维的破坏，从而导致动脉僵硬，后者可能参与正常血压模型中左心室肥大的发展。
We tested the hypothesis that a simple change in wall composition (medial calcium overload of elastic fibers) can decrease aortic elasticity. Calcium overload was produced by hypervitaminosis D plus nicotine (VDN) in the young rat. Two months later, measurement of central aortic mean blood pressure in the unanesthetized, unrestrained rat showed that the VDN rat suffered from isolated systolic hypertension but that mean blood pressure was normal. Wall thickness and internal diameter determined after in situ pressurized fixation were unchanged, as was calculated wall stress. Wall stiffness was estimated from (1) elastic modulus (determined with the Moens-Korteweg equation and values for aortic pulse wave velocity in the unanesthetized, unrestrained rat and arterial dimensions) and (2) isobaric elasticity (=slope relating pulse wave velocity to mean intraluminal pressure in the phenylephrine-infused, pithed rat preparation). Both increased after VDN, and both were significantly correlated to the wall content of calcium and the elastin-specific amino acids desmosine and isodesmosine. Left ventricular hypertrophy occurred in the VDN model, and left ventricular mass was related to isobaric elasticity. In conclusion, elastocalcinosis induces destruction of elastic fibers, which leads to arterial stiffness, and the latter may be involved in the development of left ventricular hypertrophy in a normotensive model.