Excessive Adventitial Remodeling Leads to Early Aortic Maladaptation in Angiotensin-Induced Hypertension.
Excessive Adventitial Remodeling Leads to Early Aortic Maladaptation in Angiotensin-Induced Hypertension.
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DOI：
10.1161/hypertensionaha.115.06262
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发表时间：
2016-05
期刊：
影响因子：
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通讯作者：
Humphrey JD
中科院分区：
文献类型：
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作者：
Bersi MR;Bellini C;Wu J;Montaniel KRC;Harrison DG;Humphrey JD
中央动脉的主要功能是在收缩时储存弹性能量，并在舒张期用它来维持血液流动。动脉硬化损害了这种正常的机械功能，并对终末器官如大脑、心脏和肾脏造成不利影响。在野生型小鼠中使用血管紧张素-II输注高血压模型，我们发现胸主动脉在两周内表现出显著的能量储存损失，并持续至少四周。这种机械功能的减弱是由于外膜胶原过度积累而导致的结构僵硬增加所致，而不是壁固有硬度的变化。对跨壁双轴壁应力的详细分析表明，胶原蛋白的大量产生更多地是炎症反应的结果，而不是机械适应的结果，因此加强了控制炎症的必要性，而不仅仅是血压。尽管大多数对动脉硬化的临床评估都集中在内膜-中膜增厚上，但这些结果表明有必要测量和控制高度活跃和重要的外膜。
The primary function of central arteries is to store elastic energy during systole and to use it to sustain blood flow during diastole. Arterial stiffening compromises this normal mechanical function and adversely affects end organs such as the brain, heart, and kidneys. Using an angiotensin-II infusion model of hypertension in wild-type mice, we show that the thoracic aorta exhibits a dramatic loss of energy storage within two weeks that persists for at least four weeks. This diminished mechanical functionality results from increased structural stiffening due to an excessive accumulation of adventitial collagen, not a change in the intrinsic stiffness of the wall. A detailed analysis of the transmural biaxial wall stress suggests that the exuberant production of collagen results more from an inflammatory response than a mechano-adaptation, hence reinforcing the need to control inflammation, not just blood pressure. Although most clinical assessments of arterial stiffening focus on intimal-medial thickening, these results suggest a need to measure and control the highly active and important adventitia.