Dynamic monitoring of microvessel models in time and space

首先，我们进一步将压力传感器嵌入到气腔中，对该设备进行了测量。我们还根据胶原凝胶的渗透性和弹性建立了一维分析模型来预测压力梯度的扩散。这一独特的方法使我们能够展示在压缩和拉伸条件下天然胶原蛋白凝胶的渗透性下降和应变硬化增强，这两种影响在化学交联后基本上消失。此外，我们报道了使用正弦流体注射来控制天然胶原凝胶的渗透性，这一效应可以通过拉伸和压缩的不对称响应来解释。第二，我们比较了在机械静止和腔内压力下大分子通过内皮组织的传输，并将这些数据与内皮连接的电子显微镜相关联。当施加100帕的腔内压力时，我们证明通过组织的流量增加了2.35倍。这种增加与25%的微血管直径扩张有关，这导致组织重塑和细胞旁连接变薄。我们用可变形的单孔模型概括了这些数据，在该模型中，细胞旁运输的增加是通过机械应力下通过变薄连接的扩散速率的增加来解释的。

Firstly, we went further instrumenting the device with a pressure sensor embedded into an air cavity. We also have developped an 1D analytical model to predict the diffusion of the pressure gradient according to the permeability and elasticity of collagen gel. This unique approach allowed us to show a drop in the permeability and enhanced strain-stiffening of native collagen gels under compression vs. tension, both effects being essentially lost after chemical cross-linking. Further, we report the control of the permeability of native collagen gels using sinusoidal fluid injection, an effect explained by the asymmetric response in tension and compression.Secondly, we compare the transport of macromolecules through endothelial tissues at mechanical rest or with intraluminal pressure, and correlate these data with electron microscopy of endothelial junctions. Upon application of an intraluminal pressure of 100 Pa, we demonstrate that the flow through the tissue increases by 2.35 times. This increase is associated with a 25% expansion of microvessel diameter, which leads to tissue remodeling and thinning of the paracellular junctions. We recapitulate these data with the deformable monopore model, in which the increase in paracellular transport is explained by the augmentation of the diffusion rate across thinned junctions under mechanical stress.