Abstract
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.
Highlights
Intravenous (IV) procedure involves an invasive insertion of a short peripheral catheter (SPC) into a peripherally located vein in the upper hand or forearm [1, 2]
The present study examined the effect of mechanical compression on the inflammatory response of endothelial cells (ECs) which was evaluated by the production of von Willebrand factor (vWF) and IL-8
ECs constitute the principal source for vWF and IL-8
Summary
Intravenous (IV) procedure involves an invasive insertion of a short peripheral catheter (SPC) into a peripherally located vein in the upper hand or forearm [1, 2]. We believe that the biomechanical interaction between the SPC and the vein wall promotes inflammatory response of the ECs. The SPC irritates and activates the ECs, which in response trigger a complex network of mediators and factors to initiate inflammatory processes. When released in-vivo, the folded vWF multimers are rapidly anchored to the surface of the ECs as ultra large hyperactive strings [6]. The role of these strings in pathophysiologic processes has been extensively studied [7,8,9]. It is believed that these strings contribute to inflammatory diseases such as thrombotic thrombocytopenic purpura (TTP) [9], arterial thrombosis [10], deep vein thrombosis [8], and have prothrombotic effect by promoting leukocyte and platelets adhesion and rolling on the ECs surface [7, 11]
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