超声波触发微泡破裂导致血管关闭已在肿瘤生长延迟或抑制、病变形成、放射增敏和免疫微环境调节的临床前研究中取得了非常好的效果。抗血管超声旨在作为一种局部、靶向、非侵入性、机械性和非热性的治疗方法，单独或结合其他治疗方法使用，而此综述将这些治疗方法定位在更广泛的治疗超声领域中。大范围的超声曝光条件已经报道了抗血管效应，并且证据表明空化作为主要机制发挥了显著作用。在相对较低的峰负压声压下，主要是非惯性空化，而较高的峰负压会导致惯性空化和气泡塌缩。结果生物效应以炎症和/或血管内皮下层脱开为始。后者导致组织因子进入血管内，从而引发血小板聚集和血液凝固。或者，内皮损伤暴露了亚内皮胶原层，导致血小板的快速粘附和聚集以及血液凝固。在一项临床试验中，接受超声波触发微泡破裂和经动脉放射性栓塞治疗的患者中观察到肿瘤反应占优势。目前正在进行的两项临床试验评估了超声刺激微泡治疗在增强肿瘤放射疗效方面的有效性。因此，抗血管超声/微泡方法的临床转化可能即将来临。

Ultrasound-triggered microbubbles destruction leading to vascular shutdown have resulted in preclinical studies in tumor growth delay or inhibition, lesion formation, radio-sensitization and modulation of the immune micro-environment. Antivascular ultrasound aims to be developed as a focal, targeted, non-invasive, mechanical and non-thermal treatment, alone or in combination with other treatments, and this review positions these treatments among the wider therapeutic ultrasound domain. Antivascular effects have been reported for a wide range of ultrasound exposure conditions, and evidence points to a prominent role of cavitation as the main mechanism. At relatively low peak negative acoustic pressure, predominantly non-inertial cavitation is most likely induced, while higher peak negative pressures lead to inertial cavitation and bubbles collapse. Resulting bioeffects start with inflammation and/or loose opening of the endothelial lining of the vessel. The latter causes vascular access of tissue factor, leading to platelet aggregation, and consequent clotting. Alternatively, endothelium damage exposes subendothelial collagen layer, leading to rapid adhesion and aggregation of platelets and clotting. In a pilot clinical trial, a prevalence of tumor response was observed in patients receiving ultrasound-triggered microbubble destruction along with transarterial radioembolization. Two ongoing clinical trials are assessing the effectiveness of ultrasound-stimulated microbubble treatment to enhance radiation effects in cancer patients. Clinical translation of antivascular ultrasound/microbubble approach may thus be forthcoming.© The author(s).