Farrar D J, Bond M G, Sawyer J K, Green H D
Cardiovasc Res. 1984 Feb;18(2):107-18. doi: 10.1093/cvr/18.2.107.
To determine the time course of changes in arterial stiffness and corresponding morphology during atherosclerosis progression, we determined pulse wave velocity (PWV) in cynomolgus monkeys fed atherogenic (test) and control diets over an 18-month period. At 6-month intervals, thoracic and abdominal aortic PWVs were determined with a pressure transducer retracted down the aorta in 5 cm increments. Iliac artery PWV was determined from the abdominal aortic pressure to a noninvasive femoral pulse. Groups of individual cardiac cycles, triggered by the ECGs, were sampled on a computer and the velocities (PWV) of the pulse wave fronts were calculated. There was no significant difference between groups until 18 months when test animal PWVs in the thoracic (7.44 +/- 0.83 m X s-1) and abdominal (8.52 +/- 0.67 m X s-1) aorta were significantly greater than those of controls (5.02 +/- 0.51 and 6.24 +/- 0.53 m X s-1, respectively), indicating increased arterial stiffness. There was no change in iliac PWV, 10.96 +/- 0.74 m X s-1 for 18-month test compared with 9.44 +/- 0.89 m X s-1 for controls. Constant infusion of nitroprusside and noradrenaline lowered and raised blood pressure and PWV in all groups, and PWV changes due to drug-induced pressure changes were greater in atherosclerotic than in control arteries. Systolic pressure of 18-month test and pulse pressure of 12- and 18-month test groups were significantly greater than controls under all drug conditions, also indicating increased vessel stiffness. Morphometric evaluation of histological aortic cross sections revealed early, noncomplicated atherosclerosis showing gradual increases in the ratio of intimal to medial cross-sectional area in the thoracic (1.24 +/- 0.30 after 18 months) and abdominal (1.70 +/- 0.42 after 18 months) aortas, compared with control ratios of essentially zero. The fraction of the internal elastic lamina covered with atherosclerotic lesions, and maximal intimal thickness also showed significant increases during the test diet period. These data show that early atherosclerosis resulted in aortic but not iliac stiffening which was detected by increased PWV before development of significant stenotic lesions.
为了确定动脉粥样硬化进展过程中动脉僵硬度变化的时间进程及其相应的形态学变化，我们在18个月的时间里，对喂食致动脉粥样硬化（试验）饮食和对照饮食的食蟹猴测定了脉搏波速度（PWV）。每隔6个月，用压力传感器沿主动脉以5厘米的增量回缩，测定胸主动脉和腹主动脉的PWV。从腹主动脉压力到无创股动脉脉搏测定髂动脉PWV。由心电图触发的单个心动周期组在计算机上采样，并计算脉搏波前峰的速度（PWV）。直到18个月时，试验动物胸主动脉（7.44±0.83米/秒）和腹主动脉（8.52±0.67米/秒）的PWV显著高于对照组（分别为5.02±0.51和6.24±0.53米/秒），表明动脉僵硬度增加，在此之前两组之间无显著差异。髂动脉PWV没有变化，18个月试验组为10.96±0.74米/秒，对照组为9.44±0.89米/秒。持续输注硝普钠和去甲肾上腺素可降低和升高所有组的血压和PWV，并且动脉粥样硬化组因药物诱导的压力变化导致的PWV变化大于对照组。在所有药物条件下，18个月试验组的收缩压以及12个月和18个月试验组的脉压均显著高于对照组，这也表明血管僵硬度增加。对主动脉组织学横截面的形态计量学评估显示，早期、无并发症的动脉粥样硬化表现为胸主动脉（18个月后为1.24±0.30）和腹主动脉（18个月后为1.70±0.42）内膜与中膜横截面积之比逐渐增加，而对照组的该比值基本为零。在试验饮食期间，被动脉粥样硬化病变覆盖的内弹性膜部分以及最大内膜厚度也显著增加。这些数据表明，早期动脉粥样硬化导致主动脉而非髂动脉僵硬，在显著狭窄病变出现之前，通过PWV增加即可检测到。
