Ultrasound-mediated microbubble cavitation improves perfusion in chronic limb and myocardial ischemia. The purpose of this study was to determine the effects of ultrasound-mediated microbubble cavitation in acute limb ischemia and investigate the mechanism of action. The animal with acute hindlimb ischemia was established using male Sprague-Dawley rats. The rats were randomly divided into three groups: intermittent high-mechanical-index ultrasound pulses combined with microbubbles (ultrasound [US] + MB group), US alone (US group) and MB alone (MB group). Both hindlimbs were treated for 10 min. Contrast ultrasound perfusion imaging of both hindlimbs was performed immediately and 5, 10, 15, 20 and 25 min after treatment. The role of the nitric oxide (NO) pathway in increasing blood flow in acutely ischemic tissue was evaluated by inhibiting endothelial nitric oxide synthase (eNOS) with N^ω-nitro-L-arginine methyl ester hydrochloride (L-NAME). In the US + MB group, microvascular blood volume and microvascular blood flow of the ischemic hindlimb were significantly increased after treatment (both p values <0.05), while the microvascular flux rate (β) increased, but not significantly (p > 0.05). The increases were observed immediately after treatment, and had dissipated by 25 min. Changes in the US and MB groups were minimal. Inhibitory studies indicated cavitation increased phospho-eNOS concentration in ischemic hindlimb muscle tissue, and the increase was significantly inhibited by L-NAME (p < 0.05). Ultrasound-mediated microbubble cavitation transiently increases local perfusion in acutely ischemic tissue, mainly by improving microcirculatory perfusion. The eNOS/NO signaling pathway appears to be an important mediator of the effect.

超声介导的微泡空化可改善慢性肢体和心肌缺血的灌注。本研究的目的是确定超声介导的微泡空化在急性肢体缺血中的作用并研究其作用机制。使用雄性 Sprague-Dawley 大鼠建立具有急性后肢缺血的动物。将大鼠随机分为三组：间歇性高机械指数超声脉冲联合微泡（超声[US] + MB组）、单独US（US组）和单独MB（MB组）。两条后肢均处理10分钟。在治疗后立即和 5、10、15、20 和 25 分钟对两个后肢进行对比超声灌注成像。N ^{ω -}硝基-L-精氨酸甲酯盐酸盐（L-NAME）。US+MB组缺血后肢微血管血容量和微血管血流量在治疗后显着增加（均p值<0.05），而微血管通量率（β）增加，但不显着（p >0.05）。治疗后立即观察到增加，并在 25 分钟后消散。US 和 MB 组的变化很小。抑制性研究表明空化增加了缺血后肢肌肉组织中磷酸-eNOS 的浓度，并且该增加被 L-NAME 显着抑制（p< 0.05)。超声介导的微泡空化可瞬时增加急性缺血组织的局部灌注，主要是通过改善微循环灌注。eNOS/NO 信号通路似乎是该效应的重要介质。