London G M
F.H. Manhès Hospital Centre, Fleury-Mérogis, France.
J Hypertens Suppl. 1995 Aug;13(2):S35-8. doi: 10.1097/00004872-199508001-00006.
One of the characteristics of hypertension is an impairment in arterial hemodynamics. Any definition of hypertension has to take account of oscillatory fluctuations during the cardiac cycle, that is, fluctuations in systolic and diastolic blood pressure around mean arterial pressure. These fluctuations are determined by ventricular ejection, arterial distensibility and the timing of arterial wave reflections. EFFECTS OF AGING ON LARGE ARTERIES: Larger arteries stiffen progressively with age, due to medial and intimal thickening. This alteration can be described as a decrease in arterial distensibility (Di = delta D/delta P x D, where D is the diameter of the artery and P is the blood pressure). The most obvious consequence of arterial stiffening is an increase in the amplitude of pulse pressure, caused by an increase in systolic pressure and a decrease in diastolic pressure. Two mechanisms underlie this increase in pulse pressure: a higher incident pressure wave generated by the left ventricle into a stiffened aorta and an increase in the velocity of the pressure wave traveling forward and back in the arterial tree. In young subjects, the reflected wave causes an increase in the early diastolic wave, but in older people the reflected wave is summed with a late systolic wave, causing a dramatic increase in central systolic pressure. These phenomena affect left ventricular function adversely, increasing myocardial oxygen consumption and tending to decrease coronary blood flow. Furthermore, the increased systolic blood pressure induces left ventricular hypertrophy. EFFECTS OF ANTIHYPERTENSIVE DRUGS: Although all classes of antihypertensive drugs can reduce blood pressure, only some can decrease arterial distensibility. Angiotensin converting enzyme inhibitors and calcium antagonists have been shown to decrease the stiffness of conduit arteries and dilate peripheral arteries. This may account for the superiority of these drugs in regressing left ventricular hypertrophy.
高血压的特征之一是动脉血流动力学受损。任何高血压的定义都必须考虑心动周期中的振荡波动，即收缩压和舒张压围绕平均动脉压的波动。这些波动由心室射血、动脉可扩张性和动脉波反射的时间决定。
随着年龄增长，大动脉会逐渐变硬，这是由于中膜和内膜增厚所致。这种改变可描述为动脉可扩张性降低（Di = ΔD/ΔP×D，其中D是动脉直径，P是血压）。动脉僵硬最明显的后果是脉压幅度增加，这是由收缩压升高和舒张压降低引起的。脉压增加有两个机制：左心室向僵硬的主动脉产生的入射压力波更高，以及压力波在动脉树中来回传播的速度增加。在年轻受试者中，反射波导致舒张早期波增加，但在老年人中，反射波与收缩晚期波叠加，导致中心收缩压显著升高。这些现象对左心室功能产生不利影响，增加心肌氧消耗并倾向于减少冠状动脉血流。此外，收缩压升高会导致左心室肥厚。
尽管所有类别的抗高血压药物都能降低血压，但只有一些药物能降低动脉可扩张性。血管紧张素转换酶抑制剂和钙拮抗剂已被证明可降低输送动脉的硬度并扩张外周动脉。这可能解释了这些药物在消退左心室肥厚方面的优势。
