Dobrin P B
Ann Biomed Eng. 1984;12(5):497-510. doi: 10.1007/BF02363919.
Vascular smooth muscle mechanics have been studied in vitro in cylindrical segments of dog carotid artery, human internal mammary artery, and human saphenous vein. Such cylindrical preparations maintain normal vessel geometry and also permit correlation of mechanical phenomena with transmural pressure. These studies show that the vascular muscle in cylindrical arteries develops a maximum active stress of 1.1 X 10(5) N/m2 for the whole wall, or 2.2-3.7 X 10(5) N/m2 for the volume of the wall occupied by vascular muscle. These values are similar to those reported for strip studies of vascular muscle and various preparations of skeletal muscle, but are two to five times that reported for cardiac papillary muscle preparations. In cylindrical preparations of arteries, maximum isometric active stress occurs at 150 mm Hg, whereas that in veins occurs at less than 15 mm Hg. Quick release experiments of cylindrical segments of vessels avoid the compliance of inactive tissue trapped beneath ligatures in strip studies. Quick release experiments in cylindrical segments of dog carotid artery reveal that at maximum isometric stress, the series elastic component (SEC) is extended 8-11%. Experiments employing temperature variations and degradative enzymes show that the SEC is located largely in elastin, with a lesser portion located in the contractile apparatus. At short- and long-muscle lengths, the active muscle develops decreased active stress and that developed at long lengths persists at all muscle lengths, even after shortening. This has been termed "attenuation" and appears to contribute to the static length-stress and pressure-diameter hysteresis exhibited by vessels. Excitation of vascular muscle in vessel segments held at constant pressure discloses that isobaric contraction decreases artery diameter a maximum of approximately 25%. This occurs at a dimension corresponding to approximately 100 mm Hg in the relaxed vessel. Isometrically and isobarically contracted vessels tend to fall along the same pressure-diameter coordinates, indicating equivalence of both modes of contraction. Distention of contracted vessels indicates that active vascular muscle markedly resists distention up to 150-250 mm Hg; at higher pressures the contracted vessel exhibits decreased stiffness as the contracted muscle yields. The vascular muscle, therefore, has a biphasic effect on circumferential elastic modulus relative to that of the relaxed vessel.(ABSTRACT TRUNCATED AT 400 WORDS)
血管平滑肌力学已在体外对犬颈动脉、人乳内动脉和人隐静脉的圆柱状节段进行了研究。这种圆柱状标本保持了正常的血管几何形状,还能使力学现象与跨壁压力相关联。这些研究表明,圆柱状动脉中的血管平滑肌,对于整个血管壁而言,最大主动应力为1.1×10⁵ N/m²,而对于血管平滑肌所占的血管壁体积而言,则为2.2 - 3.7×10⁵ N/m²。这些数值与血管平滑肌条带研究以及各种骨骼肌标本所报告的数值相似,但却是心脏乳头肌标本所报告数值的两到五倍。在动脉的圆柱状标本中,最大等长主动应力出现在150 mmHg时,而在静脉中则出现在低于15 mmHg时。血管圆柱状节段的快速释放实验避免了条带研究中结扎下方非活性组织的顺应性问题。犬颈动脉圆柱状节段的快速释放实验表明,在最大等长应力时,串联弹性成分(SEC)伸长了8 - 11%。采用温度变化和降解酶的实验表明,SEC主要位于弹性蛋白中,较小部分位于收缩装置中。在短肌长度和长肌长度时,活性肌肉产生的主动应力降低,且在长肌长度时产生的主动应力在所有肌肉长度下都持续存在,即使在缩短后也是如此。这被称为“衰减”,似乎导致了血管所表现出的静态长度 - 应力和压力 - 直径滞后现象。在恒压下对血管节段中的血管平滑肌进行刺激发现,等压收缩使动脉直径最大减小约25%。这发生在对应于松弛血管中约100 mmHg的尺寸时。等长收缩和等压收缩的血管倾向于沿着相同的压力 - 直径坐标下降,表明两种收缩模式等效。对收缩血管的扩张表明,活性血管平滑肌在高达150 - 250 mmHg时显著抵抗扩张;在更高压力下,随着收缩肌肉屈服,收缩血管的硬度降低。因此,相对于松弛血管,血管平滑肌对周向弹性模量具有双相作用。(摘要截断于400字)