Pulse Pressure, Arterial Stiffness, and End-Organ Damage
Pulse Pressure, Arterial Stiffness, and End-Organ Damage
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DOI：
10.1007/s11906-012-0272-9
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发表时间：
2012-08-01
影响因子：
5.6
通讯作者：
Mimran, Albert
中科院分区：
文献类型：
--
作者：
Safar, Michel E.;Nilsson, Peter M.;Mimran, Albert
较大的动脉参与抑制由间歇性心室射血引起的血压（BP）振荡，而较小的动脉稳定地从心脏向外周器官输送充足的血液供应。在这一过程中涉及许多积极的机制。循环应力的作用与稳定应力不同，导致血管壁的材料比静态条件下更强和更硬。循环应变参与平滑肌细胞的表型可塑性，启动转导机制并诱导机械诱导基因的转录谱。最后，保护脑、心脏和肾脏免受心血管（CV）损伤的自动调节机制根据其定位而显著不同。由于冠状动脉的舒张灌注，心脏依赖于脉动力，而大脑和肾脏则受到稳定机械力的影响。对于肾脏，脉动压力的传递可能极大地促进老年人肾小球硬化。
Whereas larger arteries participate in the dampening of blood pressure (BP) oscillations resulting from intermittent ventricular ejection, smaller arteries steadily deliver an adequate supply of blood from the heart to the peripheral organs. Numerous active mechanisms are involved in this process. Cyclic stress acts differently from steady stress, inducing stronger and stiffer material of the vessel wall than under static conditions. Cyclic strain participates in the phenotypic plasticity of smooth muscle cells, initiates transduction mechanisms and induces the transcriptional profile of mechanically induced genes. Finally, the autoregulatory mechanism protecting the brain, heart and kidney from cardiovascular (CV) damage differ markedly according to their localization. Whereas the heart is dependent on pulsatile forces, owing to the diastolic perfusion of coronary arteries, the brain and the kidney are rather influenced by steady mechanical forces. For the kidney, the transmission of pulsatile pressure may greatly contribute to glomerular sclerosis in the elderly.