In humans, the pathophysiological inflammation response subsequent to hypoxia and reoxygenation often leads to systemic inflammation and multiorgan failure. We applied a newly developed static interaction model using human polymorphonuclear neutrophils and microvascular endothelial cells to clarify the role of hypoxia and hypoxia/reoxygenation in vitro. Human dermal microvascular endothelial cell cultures (n = 7) were exposed to hypoxia and different reoxygenation periods and the adherence rate of neutrophils to the endothelial cells as well as to the protein matrix on the culture slide surface were determined by quantitative microscopy. Hypoxia clearly triggered neutrophil adhesion to human dermal microvascular endothelial cells whereas additional reoxygenation significantly decreased neutrophil adhesion. These in vitro findings suggest that systemic inflammation caused by increased neutrophil adherence to the microvascular endothelium is already initiated by hypoxia rather than by subsequent reoxygenation.