Fischell T A, Grant G, Johnson D E
Division of Cardiology, Stanford University Medical Center, Calif 94305.
Circulation. 1990 Dec;82(6):2170-84. doi: 10.1161/01.cir.82.6.2170.
To study the determinants of smooth muscle injury during balloon angioplasty, we conducted a series of experiments to examine the effects of degree of arterial stretching, duration of balloon inflation, and arterial precontraction on smooth muscle injury after balloon angioplasty in isolated, perfused whole-vessel segments of rabbit aortas and dog carotid arteries. Freshly dissected rabbit thoracic aortas and dog carotid arteries were mounted in a muscle bath-perfusion chamber and perfused at 80 mm Hg. The proximal half of each aorta was dilated with a 5-mm (41 +/- 6% stretch), 6-mm (64 +/- 6% stretch), or 8-mm (97 +/- 9% stretch) balloon angioplasty catheter, and the uninjured half of each vessel served as the control. The vasoconstrictor behavior of the dilated segment was then assessed by dose-response testing; long-axis, ultrasonic imaging combined with computerized edge-detection image processing was used to measure changes in segmental internal vessel diameters that were induced by phenylephrine. A similar series of experiments was performed in dog carotid arteries with 5-mm balloon catheters (42 +/- 2% stretch) to compare the susceptibility to smooth muscle injury between elastic (aortic) and muscular (carotid) arteries. Additional experiments were performed to determine the roles of prolonged (30 minutes) balloon inflation and arterial precontraction on smooth muscle injury after balloon angioplasty. In rabbit aortas, the dilated arterial segments demonstrated normal reactivity to phenylephrine after dilatation with 5- and 6-mm balloons (p = NS versus control). Severe smooth muscle injury (histopathologically) with "arterial paralysis" was observed after severe stretch (8-mm balloon) and after 5-mm balloon dilatation (46 +/- 5% stretch) in precontracted vessels. Prolonged balloon inflations did not impair aortic vasoconstrictor behavior. Dog carotid (muscular) arteries demonstrated angioplasty-induced smooth muscle injury with less severe degrees of stretch (47-52% stretch). Geometric modeling suggests that medial stretching during balloon angioplasty of diseased vessels in vivo is in the range of 15-41%.(ABSTRACT TRUNCATED AT 400 WORDS)
为研究球囊血管成形术期间平滑肌损伤的决定因素，我们进行了一系列实验，以检验动脉拉伸程度、球囊充盈持续时间和动脉预收缩对兔主动脉和犬颈动脉分离的、灌注的全血管段球囊血管成形术后平滑肌损伤的影响。新鲜解剖的兔胸主动脉和犬颈动脉被置于肌肉浴灌注室中，并在80毫米汞柱压力下进行灌注。每个主动脉的近端一半用5毫米（拉伸41±6%）、6毫米（拉伸64±6%）或8毫米（拉伸97±9%）球囊血管成形术导管进行扩张，每个血管未受损的一半作为对照。然后通过剂量反应测试评估扩张段的血管收缩行为；使用长轴超声成像结合计算机边缘检测图像处理来测量由去氧肾上腺素引起的节段性血管内径变化。在犬颈动脉中使用5毫米球囊导管（拉伸42±2%）进行了一系列类似实验，以比较弹性（主动脉）和肌性（颈动脉）动脉对平滑肌损伤的易感性。还进行了其他实验，以确定延长（30分钟）球囊充盈和动脉预收缩对球囊血管成形术后平滑肌损伤的作用。在兔主动脉中，用5毫米和6毫米球囊扩张后，扩张的动脉段对去氧肾上腺素表现出正常反应性（与对照相比，p = 无显著性差异）。在预收缩的血管中，严重拉伸（8毫米球囊）和5毫米球囊扩张（拉伸46±5%）后观察到严重的平滑肌损伤（组织病理学）伴“动脉麻痹”。延长球囊充盈并未损害主动脉血管收缩行为。犬颈动脉（肌性）动脉在拉伸程度较轻（拉伸47 - 52%）时表现出血管成形术诱导的平滑肌损伤。几何模型表明，体内病变血管球囊血管成形术期间的中膜拉伸范围为15 - 41%。（摘要截取自400字）
