The clinical observation of distinct reduction of wound secretion tendency during treatment of venous leg ulcer with topically applied factor XIII let us speculate that this enzyme may be involved in modulation of vascular permeability.For experimental study porcine aortic endothelial cells were cultured on filter membrane to confluent monolayer. Endothelial covered filters then were used in a two-compartment modell creating an artificial luminal and abluminal compartment. To investigate the influence of factor XIII on endothelial barrier function, we measured the flux of trypan blue-labeled albumin through endothelial monolayers by spectrophotometer.Monolayers that were exposed to factor XIII showed a distinct (n = 10, p < 0.05) decrease of albumin flux in contrast to control. This effect was not dependent on serum substrates. Partially, the permeability reducing effect was due to a certain amount of albumin that is a stabilizing component of Fibrogammin HS.Although the mechanism is unclear at the moment, we conclude that reduction of endothelial permeability can be achieved by factor XIII which may play an important role in wound healing of venous leg ulcer.