The acute inflammatory reaction constitutes the first line of defense against noxious stimuli and represents the initial phase in the healing process following tissue injury. Changes at the microcirculatory level, namely increased local blood flow, enhanced microvessel permeability, and recruitment of circulating leukocytes, are characteristics of the inflammatory response and give rise to the clinical signs of inflammation–redness, heat, swelling and pain. The physiological fluid exchange and solute transport between blood and tissue is strictly controlled by the selective barrier capacity of the endothelium [1]. In normal conditions, the permeability to macromolecules is restricted whereas water and small solutes pass freely across the microvascular barrier under homeostatic control by the hydrostatic and colloid osmotic pressures in intra-and extravascular compartments. In inflammation, the endothelial barrier is compromised and becomes more permissive for the exchange of large molecules, leading to efflux of plasma proteins from the vasculature and subsequent edema formation. It has been known for a long time that a number of inflammatory mediators, eg histamine, bradykinin and the cysteinyl leukotrienes, through direct interaction with their receptors on the endothelial cell (EC), have the capacity to induce such permeability changes in the postcapillary venules of the microvasculature. However, it has become increasingly clear that the loss of the integrity of the endothelial barrier may also occur in conjunction with leukocyte trafficking across the vessel wall. Several in vivo studies have shown that extravasation of neutrophil granulocytes is associated with an increase in vascular permeability [2–6]. Moreover, it is evident from these observations that the capacity of various chemoattractants to induce hyperpermeability depends entirely on the presence of neutrophils, or more exactly, an intact