Carretta R, Bardelli M, Cominotto F, Ussi D, Fazio M, Fabris B, Fischetti F, Campanacci L
Istituto di Medicina, University of Trieste, Italy.
J Hypertens. 1996 Sep;14(9):1105-10. doi: 10.1097/00004872-199609000-00010.
To evaluate the relationship between the mechanical properties of the carotid artery wall and baroreflex function after acute reduction of blood pressure with lacidipine in essential hypertension.
After 15 days of placebo washout, the hypertensive patients underwent a single-blind haemodynamic study before and 90 min after administration of 4 mg lacidipine (a dihydropyridine calcium antagonist).
Brachial intra-arterial blood pressure was recorded in eight mild-to-moderate essential hypertensive patients aged 40-53 years (mean +/- SEM 46.8 +/- 4.7 years). The carotid pulse diameter was recorded simultaneously by an echo-tracking technique. The mechanical properties of the carotid artery wall were evaluated by calculating Peterson's incremental elastic modulus (Ep) both as an averaged value of 10 heart cycles with stable blood pressure and was the dynamic correlation, on a beat-to-beat basis, of Ep and the systolic blood pressure during a 20 mmHg increase in blood pressure following a bolus injection of phenylephrine. The elastic properties of the carotid artery were investigated further by determining the correlation between the systolic pressure and systolic diameter, beat by beat, during a ramped increase of blood pressure after phenylephrine administration. The baroreceptor reflex sensitivity was measured simultaneously by the Oxford method and by correlating Ep and the electrocardiographic R-R' interval on a beat-to-beat basis during phenylephrine injections.
After lacidipine administration Peterson's elastic modulus, measured under resting steady-state conditions, was reduced (18.7 +/- 7.4 versus 16.4 +/- 6 x 10(5) dyne/cm2), whereas the baroreflex sensitivity was unchanged (6.6 +/- 3.3 versus 6.3 +/- 0.2 ms/mmHg) and resetting of the baroreflex had occurred. At the same time, the correlations between the systolic blood pressure and Ep and between the systolic blood pressure and carotid systolic diameter over a 20 mmHg increase in blood pressure were unchanged. Moreover, the correlations between the systolic blood pressure and the R-R' interval and between Ep and R-R' interval during the phenylephrine-induced blood pressure increase did not differ statistically.
The results suggest that the resetting of the baroreflex after the acute reduction in blood pressure caused by lacidipine is dissociated from mechanical changes in the carotid artery wall.
评估在原发性高血压患者中，拉西地平急性降压后颈动脉壁力学特性与压力反射功能之间的关系。
在停用安慰剂15天后，高血压患者在服用4mg拉西地平（一种二氢吡啶类钙拮抗剂）之前及之后90分钟进行了一项单盲血流动力学研究。
记录了8名年龄在40 - 53岁（平均±标准误46.8±4.7岁）的轻度至中度原发性高血压患者的肱动脉内血压。同时通过回声跟踪技术记录颈动脉脉搏直径。通过计算彼得森增量弹性模量（Ep）评估颈动脉壁的力学特性，Ep既作为血压稳定时10个心动周期的平均值，也是在静脉注射去氧肾上腺素使血压升高20mmHg期间，Ep与收缩压的逐搏动态相关性。通过确定去氧肾上腺素给药后血压逐渐升高期间，收缩压与收缩直径之间逐搏的相关性，进一步研究颈动脉的弹性特性。在注射去氧肾上腺素期间，同时采用牛津法并通过逐搏关联Ep与心电图R - R'间期来测量压力感受器反射敏感性。
服用拉西地平后，在静息稳态条件下测量的彼得森弹性模量降低（18.7±7.4对16.4±6×10⁵达因/平方厘米），而压力反射敏感性未改变（6.6±3.3对6.3±0.2毫秒/毫米汞柱），并且发生了压力反射重调定。同时，在血压升高20mmHg时，收缩压与Ep之间以及收缩压与颈动脉收缩直径之间的相关性未改变。此外，在去氧肾上腺素引起血压升高期间，收缩压与R - R'间期之间以及Ep与R - R'间期之间的相关性在统计学上无差异。
结果表明，拉西地平引起急性血压降低后压力反射的重调定与颈动脉壁的力学变化无关。
