Dynamics of bubble oscillation in constrained media and mechanisms of vessel rupture in SWL
Dynamics of bubble oscillation in constrained media and mechanisms of vessel rupture in SWL
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DOI：
10.1016/s0301-5629(00)00322-7
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发表时间：
2001-01-01
影响因子：
2.9
通讯作者：
Zhu, SL
中科院分区：
文献类型：
--
作者：
Zhong, P;Zhou, YF;Zhu, SL
小血管破裂是与冲击波碎石术（SWL）相关的血管损伤的主要特征，并且空化被认为是一种潜在的机制。为了更精确地理解损伤的潜在机械原因，研究了受约束介质中SWL诱导的气泡动力学。使用不同内径（0.2至1.5 mm）的硅胶管和再生纤维素中空纤维制造血管体模，将其放置在充满蓖麻油的试验室中，以抑制体模外部的空化。在血管体模内循环接种0.2%Albunex（R）造影剂的脱气水，并通过20 MHz聚焦换能器的高速阴影成像和被动空化检测检查SWL期间的腔内气泡动力学。据观察，与自由场中SWL诱导气泡的典型大而长时间膨胀和剧烈惯性塌陷形成对比，血管体模内气泡的膨胀受到显著约束，导致气泡沿着血管轴不对称伸长，并可能导致塌陷减弱。约束的严重性是血管尺寸相关的，并且当血管的内径变得小于300 μ m时显著增加。相反，气泡的快速、大的管腔内膨胀引起血管壁的显著扩张，导致中空纤维的一致破裂（i.d. 200 μ m）。破裂是剂量依赖性的，并且随着在碎石机场中的血管体模的空间位置而变化。此外，当通过使碎石机压力波形反转来抑制大的管腔内气泡膨胀时，即使在100次冲击之后也可以避免中空纤维的破裂。血液中SWL诱导的气泡动力学的理论计算证实，由于腔内气泡膨胀导致的血管损伤的倾向随着碎石机冲击波的拉伸压力以及血管内径的减小而增加。有人建议，选择性截断的冲击波的拉伸压力可以减少组织损伤，而不损害碎石机脉冲的破碎能力。（电子邮件：pzhong@acpub.duke.edu）（C）2001年世界医学和生物学超声联合会。
Rupture of small blood vessels is a primary feature of the vascular injury associated with shock-wave lithotripsy (SWL) and cavitation has been implicated as a potential mechanism. To understand more precisely the underlying mechanical cause of the injury, the dynamics of SWL-induced bubble dynamics in constrained media were investigated. Silicone tubing and regenerated cellulose hollow fibers of various inner diameters (0.2 to 1.5 mm) were used to fabricate vessel phantoms, which were placed in a test chamber filled with castor oil so that cavitation outside the phantom could be suppressed. Degassed water seeded with 0.2% Albunex(R) contrast agent was circulated inside the vessel phantom, and intraluminal bubble dynamics during SWL were examined by high-speed shadowgraph imaging and passive cavitation detection via a 20-MHz focused transducer. It was observed that, in contrast to the typical large and prolonged expansion and violent inertial collapse of SWL-induced bubbles in a free field, the expansion of the bubbles inside the vessel phantom was significantly constrained, leading to asymmetric elongation of the bubbles along the vessel axis and, presumably, much weakened collapse. The severity of the constraint is vessel-size dependent, and increases dramatically when the inner diameter of the vessel becomes smaller than 300 mum. Conversely, the rapid, large intraluminal expansion of the bubbles causes a significant dilation of the vessel wall, leading to consistent rupture of the hollow fibers (i.d. 200 mum) after less than 20 pulses of shock wave exposure in a XL-1 lithotripter. The rupture is dose-dependent, and varies with the spatial location of the vessel phantom in the lithotripter field. Further, when the large intraluminal bubble expansion was suppressed by inversion of the lithotripter pressure waveform, rupture of the hollow fiber could be avoided even after 100 shocks. Theoretical calculation of SWL-induced bubble dynamics in blood confirms that the propensity of vascular injury due to intraluminal bubble expansion increases with the tensile pressure of the lithotripter shock wave, and with the reduction of the inner diameter of the vessel. It is suggested that selective truncation of the tensile pressure of the shock wave may reduce tissue injury without compromising the fragmentation capability of the lithotripter pulse. (E-mail: pzhong@acpub.duke.edu) (C) 2001 World Federation for Ultrasound in Medicine & Biology.