Cabrera Fischer E I, Armentano R L, Levenson J, Barra J G, Morales M C, Breitbart G J, Pichel R H, Simon A
INSERM U28, Hôpital Broussais, Paris, France.
Circ Res. 1991 Jun;68(6):1549-59. doi: 10.1161/01.res.68.6.1549.
We studied the aortic elastic behavior in response to vitamin D3-induced accelerated calcinosis in conscious dogs chronically instrumented with a pressure microtransducer and a pair of ultrasonic diameter dimension gauges in the upper descending thoracic aorta. The two functional phases of the elastic segmental properties of the aorta in vivo were discriminated by computation on a beat-by-beat basis from the phasic pressure-diameter (P-D) hysteresis loops in basal conditions and during the transient state of a wide range of pressures obtained mechanically (aortic occlusion) or pharmacologically (angiotensin bolus). The overall P-D curve formed by all P-D hysteresis loops was comprised of two linear relations according to a model that assumes that only elastin is stretched at lower pressures, whereas both elastin and collagen are stretched at higher pressures. The slope of the first linear portion of the P-D curve was considered as the elastin P-D elastic modulus, and the slope of the curve obtained by subtraction between the P-D curve and the extrapolation of the elastin straight line was assumed to be the collagen P-D elastic modulus. After vitamin D3-induced calcinosis, the elastin elastic modulus was unaffected, whereas the collagen elastic modulus decreased significantly during occlusion maneuvers (58.6%, p less than 0.01) and during bolus injections of angiotensin (37.2%, p less than 0.05). The collagen elastic modulus correlated with the serum calcium concentration (r = -0.65, p less than 0.001) and with the aortic pulse pressure (r = 0.51, p less than 0.01), and this relation persisted at constant heart rate. Histopathologic analysis evidenced calcium-depositing elastic lamina, focal disappearance of collagen, and rupture of elastic fibers. The present study shows that accelerated, severe, experimental calcinosis-inducing calcium deposition inside the large artery walls is accompanied by a clear-cut paradoxical reduction in arterial rigidity that is mainly due to functional and structural modification of collagen elasticity.
我们对长期植入压力微型传感器和一对位于胸主动脉上段降主动脉的超声直径测量仪的清醒犬，研究了维生素D3诱导的加速钙化时主动脉的弹性行为。通过基于逐搏计算，从基础状态下以及机械性（主动脉阻断）或药理学（血管紧张素推注）获得的广泛压力瞬态状态下的相位压力-直径（P-D）滞后环，区分了体内主动脉弹性节段特性的两个功能阶段。根据一个模型，所有P-D滞后环形成的总体P-D曲线由两个线性关系组成，该模型假定在较低压力下只有弹性蛋白被拉伸，而在较高压力下弹性蛋白和胶原蛋白都被拉伸。P-D曲线第一线性部分的斜率被视为弹性蛋白P-D弹性模量，通过P-D曲线与弹性蛋白直线外推值相减得到的曲线斜率被假定为胶原蛋白P-D弹性模量。维生素D3诱导钙化后，弹性蛋白弹性模量未受影响，而在阻断操作期间（降低58.6%，p<0.01）和血管紧张素推注期间（降低37.2%，p<0.05），胶原蛋白弹性模量显著降低。胶原蛋白弹性模量与血清钙浓度（r = -0.65，p<0.001）和主动脉脉压（r = 0.51，p<0.01）相关，并且这种关系在心率恒定的情况下持续存在。组织病理学分析显示有钙沉积的弹性膜、胶原蛋白的局灶性消失和弹性纤维的断裂。本研究表明，在大动脉壁内加速、严重的实验性钙化诱导的钙沉积伴随着动脉僵硬度明显的矛盾性降低，这主要是由于胶原蛋白弹性的功能和结构改变所致。
