Weiss Dar, Avraham Sharon, Guttlieb Ruth, Gasner Lee, Lotman Alina, Rotman Oren M, Einav Shmuel
Department of Biomedical Engineering, Faculty of Engineering, Tel Aviv University, Tel Aviv, Israel.
Department of Biomedical Engineering, Stony Brook University, Stony Brook, New York, United States of America.
PLoS One. 2017 Jan 12;12(1):e0169752. doi: 10.1371/journal.pone.0169752. eCollection 2017.
Short peripheral catheters are ubiquitous in today's healthcare environment enabling effective delivery of fluids and medications directly into a patient's vasculature. However, complications related to their use, such as short peripheral catheter thrombophlebitis (SPCT), affect up to 80% of hospitalized patients. While indwelling within the vein, the catheters exert prolonged constant pressure upon the endothelium which can trigger inflammation processes. We have developed and studied an in-vitro model of cultured endothelial cells subjected to mechanical compression of modular self-designed weights, and explored their inflammatory response by quantification of two key biomarkers- vWF and IL-8. Evaluation was performed by ELISA immunoassay and processing of vWF-labeled immunofluorescence images. We found that application of weights correspond to 272 Pa yielded increased release of vWF and IL-8 up to 150% and 250% respectively, comparing to the exertion of 136 Pa. Analyses of the immunofluorescence images revealed significantly longer and more extracellular vWF-strings as well as higher intensity stained-pixels in cells exposed to elevated pressures. The release of both factors found to be significantly dependent on the extent of the exerted pressure. The research shed a light on the relationship between induced mechanical compression and the pathogenesis of SPCT. Minimizing, let alone eliminating the contact between the catheter and the vein wall will mitigate the pressure acting on the endothelium, thereby reducing the secretion of inflammatory factors and lessen the incidence of SPCT.
在当今的医疗环境中，短外周导管随处可见，它能够将液体和药物直接有效地输送到患者的血管系统中。然而，与使用短外周导管相关的并发症，如短外周导管血栓性静脉炎（SPCT），影响着高达80%的住院患者。导管留置在静脉内时，会对内皮细胞施加持续的长时间压力，这可能引发炎症过程。我们开发并研究了一种体外模型，即利用模块化自行设计的重物对培养的内皮细胞进行机械压缩，并通过量化两种关键生物标志物——血管性血友病因子（vWF）和白细胞介素-8（IL-8）来探究它们的炎症反应。通过酶联免疫吸附测定（ELISA）和对vWF标记的免疫荧光图像进行处理来进行评估。我们发现，与施加136帕的压力相比，施加相当于272帕的重物时，vWF和IL-8的释放量分别增加了150%和250%。对免疫荧光图像的分析显示，在承受较高压力的细胞中，vWF链明显更长且更多地分布在细胞外，同时染色像素的强度也更高。发现这两种因子的释放都显著依赖于所施加压力的程度。该研究揭示了诱导机械压缩与SPCT发病机制之间的关系。尽量减少，更不用说消除导管与静脉壁之间的接触，将减轻作用在内皮细胞上 的压力，从而减少炎症因子的分泌并降低SPCT的发生率。
