Spotlight on microvascular permeability.

摘要

The normal endothelium forms a stable anti-inflammatory, anti-thrombotic, and anti-adhesive interface between circulating blood components and cells within all tissues of the body. The endothelium and its associated structures, e.g. glycocalyx, basement membrane, and pericytes, form the primary barrier to water and plasma protein exchange. This barrier is sufficient to maintain the plasma volume and venous return, and prevent tissue oedema while it enables transvascutar exchange to meet metabolic and homeostatic demands of the tissues. Under normal physiological conditions, an increase in the amount of nutrient exchange is most probably the result of vasodilation to increase the surface area and the driving forces for water (microvessel pressure) and solute exchange (concentration differences) without a significant increase in permeability.1'2 The view of the endothelium as a stable barrier allowing selective exchange of water, nutrients, and plasma proteins stands in contrast to the other well-recognized role of the endothelial barrier as a major player in inflammatory processes in which the components of the normal barrier, iacludingthe surface glycocalyx and the junctions between adjacent endothelial cells, are acutely or permanently modified as part of immune responses and, at the same time, compromise barrier function. In this case, vasodilation caused by inflammatory mediators or clinical interventions only exacerbates the dysfunctional state. Thus, microvas-cular exchange is modulated not only by changes in the conductance of the endothelial barrier (measured as a real change in microvascular permeability) but also by local perfusion conditions. The reviews covered in this Spotlight Issue provide a broad survey on many fundamental aspects of the control of microvascular exchange processes under both physiological and pathological conditions.