Glaser E, Lacolley P, Boutouyrie P, Sacunha R, Lucet B, Safar M E, Laurent S
Department of Internal Medicine, INSERM (U 337), Broussais Hospital, Paris, France.
J Vasc Res. 1995 Jul-Aug;32(4):254-65. doi: 10.1159/000159100.
Arteries, when they are subjected in vitro to cyclic loading and unloading, are reported to be stiffer than in static conditions and to be poorly influenced by changes in vasomotor tone. However, such parameters have never been studied in living animals. This study used very high resolution echotracking technics to evaluate pulsatile changes of carotid blood pressure and diameter and the resulting dynamic pressure-cross-sectional (CSA) curve in anesthetized Wistar-Kyoto rats before and following changes of arteriolar vasomotor tone produced by vasoconstrictive [phenylephrine, L-NG nitro-arginine (LNA)] or vasodilating (hydralazine, nitroprusside) agents. Phenylephrine and LNA caused a progressive upward shift of the pressure-CSA curve toward significantly higher values of mean blood pressure and diameter. Since the two vasoconstrictive agents produced exactly the same arterial hemodynamic pattern, their effects may be considered as 'passive', i.e. predominantly due to the mechanical effect of pressure distension. From this observation, a simple model was validated, permitting evaluation in vivo of the passive static properties of the pressure-CSA curve from the relationship between mean arterial diameter and mean arterial pressure at the various steady states produced by the two vasoconstrictive agents. This static relationship had a significantly steeper slope than the corresponding dynamic relationships determined for the same steady-state mean arterial pressures. With hydralazine, a downward shift of the pulsatile pressure-CSA curve was obtained, with exactly the same characteristics as for phenylephrine and LNA, but within lower ranges of blood pressure and with a corresponding decrease in arterial diameter. In contrast, nitroprusside shifted the pulsatile pressure diameter curve toward both lower values of blood pressure and higher values of arterial diameter, thus indicating an active change in arterial tone. At any given value of mean blood pressure and arterial diameter, operational pulsatile compliance was significantly higher with sodium nitroprusside than with hydralazine. This study provides evidence that in living rats (1) the described static carotid pressure-diameter curve has a significantly steeper slope than the corresponding dynamic curve for the same mean arterial pressure, (2) for the same mean arterial pressure and diameter, sodium nitroprusside has a significantly higher dynamic compliance than hydralazine, implicating the role of nonhemodynamic factors in the stiffness of changes, and (3) vasomotor tone influences markedly the dynamic pressure-diameter (or CSA) curve within intermediate and lower blood pressure ranges through active mechanisms involving the GMP cyclic pathway.
据报道，动脉在体外进行周期性加载和卸载时，比在静态条件下更硬，且血管舒缩张力的变化对其影响较小。然而，这些参数从未在活体动物中进行过研究。本研究使用超高分辨率回声跟踪技术，评估麻醉的Wistar-Kyoto大鼠在使用血管收缩剂[去氧肾上腺素、L-NG硝基精氨酸（LNA）]或血管扩张剂（肼屈嗪、硝普钠）改变小动脉血管舒缩张力之前和之后，颈动脉血压和直径的脉动变化以及由此产生的动态压力-横截面积（CSA）曲线。去氧肾上腺素和LNA使压力-CSA曲线逐渐向上移动，朝着平均血压和直径显著更高的值变化。由于这两种血管收缩剂产生了完全相同的动脉血流动力学模式，它们的作用可被视为“被动的”，即主要是由于压力扩张的机械效应。基于这一观察结果，验证了一个简单的模型，该模型允许根据两种血管收缩剂在不同稳态下产生的平均动脉直径与平均动脉压力之间的关系，在体内评估压力-CSA曲线的被动静态特性。这种静态关系的斜率比在相同稳态平均动脉压力下确定的相应动态关系的斜率明显更陡。使用肼屈嗪时，脉动压力-CSA曲线向下移动，其特征与去氧肾上腺素和LNA完全相同，但血压范围较低，动脉直径相应减小。相比之下，硝普钠使脉动压力-直径曲线朝着血压较低值和动脉直径较高值移动，从而表明动脉张力发生了主动变化。在任何给定的平均血压和动脉直径值下，硝普钠的操作脉动顺应性显著高于肼屈嗪。本研究提供的证据表明，在活体大鼠中：（1）所描述的静态颈动脉压力-直径曲线的斜率比相同平均动脉压力下的相应动态曲线明显更陡；（2）对于相同的平均动脉压力和直径，硝普钠的动态顺应性显著高于肼屈嗪，这表明非血流动力学因素在血管硬度变化中起作用；（3）血管舒缩张力通过涉及GMP循环途径的主动机制，在中、低血压范围内显著影响动态压力-直径（或CSA）曲线。
