血管生成反应依赖于超声造影剂浓度。

Q4 Neuroscience
Chenara A Johnson, William D O'Brien
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引用次数: 4

摘要

目的:超声(US)和超声造影剂(UCAs)提供了一种无创诱导靶向血管生成的方法。然而,对这一进程的机制缺乏了解,阻碍了进展。本研究试图通过探索暴露后0天(DPE)时UCA浓度([UCA])在生物效应诱导中的作用,以及评估暴露后5天(DPE)时生物效应作为血管生成可能的增强剂的作用,来表征血管生成反应。方法:采用1 mhz超声换能器,脉冲持续时间10 μs,脉冲重复频率10 hz,峰值相对声压(pr) 0.7 mpa,暴露大鼠股薄肌5 min。测试了四种[UCA]: 0x(生理盐水),1x, 5x和10x,其中1x为5%的溶液体积清晰度。用Evans蓝染料(EBD)量化急性血管通透性(0 DPE)的变化,并在5 DPE时量化VEGF表达,以支持血管新生的发生。CD31染色评估两个时间点的毛细血管密度。结果:[UCA]是确定EBD渗漏(通透性)和VEGF表达的重要参数(p)。结论:本研究提示[UCA]是诱导US和UCA血管生成反应的重要参数。它还表明,与之前推测的由US和uca造成的损伤不同,uca和血管内皮之间的非破坏性机械相互作用诱导了生物效应,从而增强了血管生成反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The angiogenic response is dependent on ultrasound contrast agent concentration.

The angiogenic response is dependent on ultrasound contrast agent concentration.

The angiogenic response is dependent on ultrasound contrast agent concentration.

The angiogenic response is dependent on ultrasound contrast agent concentration.

Objective: Ultrasound (US) and ultrasound contrast agents (UCAs) provide a way to noninvasively induce targeted angiogenesis. However, there exists a lack of understanding regarding the mechanisms of this process that has impeded progress. This study sought to characterize the angiogenic response, by both exploring the role of UCA concentration ([UCA]) in bioeffect induction at 0 days post exposure (DPE) and assessing the bioeffect as a possible potentiator of angiogenesis at 5 DPE.

Methods: A 1-MHz ultrasonic transducer was used to expose the gracilis muscles of Sprague Dawley rats for 5 min with a 10-μs pulse duration, 10-Hz pulse repetition frequency, and 0.7-MPa peak rarefactional acoustic pressure (pr). Four [UCA]s were tested: 0x (saline), 1×, 5×, and 10×, where 1× is 5% Definity by volume of solution. Evans blue dye (EBD) was used to quantify changes in acute vascular permeability (0 DPE), and VEGF expression was quantified at 5 DPE to support that angiogenesis had occurred. CD31 staining was used to assess capillary density at both time points.

Results: [UCA] was a significant parameter for determining EBD leakage (permeability) and VEGF expression (p < 0.001 for both). However, [UCA] was not a significant parameter for capillary density at 0 or 5 DPE. Multiple comparisons between 0 and 5 DPE showed that only 10× [UCA] at 5 DPE was significantly different than 0 DPE, suggesting a [UCA] dependence of the angiogenic response.

Conclusions: This study suggests that [UCA] was a significant parameter in the induction of an angiogenic response with US and UCAs. It also suggests that rather than damage from US and UCAs, as previously speculated, a nondestructive mechanical interaction between the UCAs and vascular endothelium induces bioeffects to potentiate the angiogenic response.

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来源期刊
Vascular Cell
Vascular Cell Neuroscience-Neurology
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