Aortic hypertrophy and "waterlogging" in the development of coarctation hypertension.

Aortic hypertrophy and "waterlogging" in the development of coarctation hypertension.
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主动脉肥大和缩窄性高血压发展中的“积水”。

DOI:
10.1161/01.hyp.14.3.316
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发表时间:
1989
期刊:
Hypertension (Dallas, Tex. : 1979)
影响因子:
--
通讯作者:
Magargal,WW
Magargal,WW
中科院分区:
--
文献类型:
--
作者:
Overbeck,HW;Magargal,WW

文献摘要

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为了研究高血压发生过程中血管结构变化的机制和作用,我们对大鼠腹主动脉进行了缩窄或假缩窄。每隔3至56天,我们获得标准化的胸主动脉和腹主动脉段,用于测量干重、含水量和氨基酸含量。缩窄大鼠颈动脉压在第5天升高,并保持升高。股动脉和尾动脉压保持正常。缩窄大鼠心室重量和胸主动脉干重(按体重归一化)在3-10天内迅速上升,此后保持在比假缩窄大鼠高50-60%的水平。相比之下,收缩大鼠的胸主动脉含水量在第7天达到峰值,为对照组的123% (p < 0.001),此后迅速下降至峰值的一半左右。正常血压的腹主动脉段干重和含水量的增加幅度要小得多,发生在1至2周后,可能反映了最初的后躯低血压的影响。在8周期间,胸主动脉内膜-中膜段的羟脯氨酸百分比保持正常,表明主动脉干重的增加并不代表不成比例的纤维化,因此可归因于肌肉肥大。这些结果支持了动脉壁“内涝”主要是高血压过程的早期表现的假设。内涝的最大程度与主动脉干重的早期快速增加一致,表现为肥厚,这提示了常见的机制,如Na+-H+反端口的激活。
To study the mechanisms and roles of vascular structural changes during the development of hypertension, we coarcted or sham-coarcted the abdominal aorta of rats. At intervals of 3 to 56 days later, we obtained standardized segments of thoracic and abdominal aortas for measurement of dry weight, water content, and amino acid content. Carotid arterial pressure was elevated by day 5 in coarcted rats and remained elevated. Femoral and tail arterial pressures remained normal. Cardiac ventricular weight and dry weight of the thoracic aorta, normalized for body weight, rose rapidly over 3-10 days in coarcted rats, remaining constant at 50-60% above levels in sham-coarcted rats thereafter. In contrast, water content of thoracic aorta in coarcted rats peaked at 123% of control values on day 7 (p less than 0.001), falling rapidly thereafter to levels about half of peak. Increments in dry weight and water content of the normotensive abdominal aortic segments were of far lesser magnitude and occurred 1 to 2 weeks later, probably reflecting the effects of initial hypotension of the hindquarters. Percent hydroxyproline of intima-media segments of the thoracic aorta remained normal during the 8-week period, indicating that increases in aortic dry weight did not represent disproportional fibrosis and thus are attributable to muscular hypertrophy. These results provide support for the hypothesis that arterial wall "waterlogging" is primarily an early manifestation of the hypertensive process. The greatest magnitude of waterlogging coincides with the rapid early increase in aortic dry weight, representing hypertrophy, which suggests common mechanisms, such as activation of Na+-H+ antiport.