REGULATION OF SINGLE CAPILLARY PERMEABILITY PROPERTIES

溶质交换的短期调节，这一过程依赖于 微血管通透性、表面积、血流量和压力，是一种 复杂的过程 复杂性变得明显，当它被证明， 毛细血管屏障是一种动态结构， 内皮细胞（EC）既是刺激的感受器， 机械换能器在调节血管张力。 鉴于这些 数据，本研究旨在评估EC在 外汇监管。 核心假设是， 屏障，特别是EC，迅速和选择性地介导 溶质渗透性随局部环境变化而变化。 目的是通过以下方式测量小溶质和蛋白质通量Js： 蛙和仓鼠血浆灌注微血管的显微荧光测定 肠系膜： 1)在原位评估后，作为灌注压的函数 剪切应力和随后的剪切应力变化，以确定是否 微容器中的流动限定了溶质的基础渗透性。 来自J 数据的传输系数，溶质渗透性（Pd）和溶剂阻力 Jv（1-sigma））。 假设是，Js将与 具有原位剪应力，特别是小的溶质渗透率， 大分子溶剂的阻力将随着剪切应力的增加而增加。 2)在基础条件下，并再次在灌注期间用一组 血管扩张剂，以确定渗透性是否对EC依赖性 和EC非依赖性血管扩张剂对于不同浓度的溶质是等效的。 尺寸 假设扩张器会增加Js，因为 扩张剂引起不同的细胞介导的屏障结构的变化， 变化将具有不同的空间和时间特征。 3)在对照条件下，再次在心房灌注期间， 利钠肽，心钠素，和第三次与心钠素后，改变 剪切应力，以确定微血管血流史是否会改变 对所选血管扩张剂的反应的幅度，反之亦然。 的 假设ANP引起的Js变化减弱了 而不是相反。 本研究的长期目标是确定 微血管渗透性特性响应于生理学变化而变化。 刺激。 调节屏障性能和Starling的能力 力量促进了交换中快速的、选择性的、局部化的变化， 交换能力，以维持体内平衡。 从长远来看， 快速稳态机制已被广泛研究， 明白 关于《公约》的监管特点， 短期（几分钟到几小时）将液体平衡控制在 交换壁垒。

Short term regulation of solute exchange, a process dependent on microvessel permeability, surface area, blood flow, and pressure, is a complex process. The complexity became evident when it w as shown that the capillary barrier was a dynamic structure responsive to a variety of stimuli and that the endothelial cell (EC) was both sensor and mechanotransducer in the regulation of vascular tone. In light of these data the present study was designed to evaluate the role of ECs in the regulation of exchange. The central hypothesis is that the exchange barrier, especially the EC, rapidly and selectively mediates changes in permeability to solute in response to changes in the local environment. The aims are to measure small solute and protein flux, Js, by microfluorometry in plasma perfused microvessels in the frog and hamster mesentery: 1) as a function of perfusion pressure, following assessment of in situ shear stress and following changes in shear stress to determine whether flow in the microvessel defines basal permeability to solute. From the Js data the transport coefficients, solute permeability (Pd) and solvent drag Jv(1-sigma)), will be calculated. The HYPOTHESIS is that Js will correlate with in situ shear stress, specifically small solute permeability and macromolecule solvent drag will increase with increasing shear stress. 2) under basal conditions and again during perfusion with a set of vasodilators to determine whether permeability responses to EC-dependent and EC-independent vasodilators are equivalent for solutes of differing size. The HYPOTHESIS is that the dilators will increase Js and because dilators evoke different cell-mediated changes in barrier structure, the js changes will have distinct spatial and temporal signatures. 3) under control conditions, again during perfusion with atrial natriuretic peptide, ANP, and third time with the ANP following a change in shear stress to determine whether mirovessel flow history modifies the magnitude of the response to a selected vasodilator and vice versa. The HYPOTHESIS is that the Js changes induced by ANP attenuate changes induced by shear-stress and not the reverse. The long term aim of this research is to determine the mechanisms whereby microvessel permeability properties vary in response to physiological stimuli. The ability to regulate both barrier properties and Starling Forces facilitates rapid, selective, localized changes in exchange in exchange capacity to maintain homeostasis. The longer term and the very fast homeostatic mechanisms have been studied extensively and are better understood. Little work has been carried out on the regulatory features in the short term (minutes to hours) control of fluid balance at the level of the exchange barrier.