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Hypoxia-Induced Activation of Endothelial Cells as a Possible Cause of Venous Diseases: Hypothesis

Laboratoire de Biochimie Cellulaire, Facultés Universitaires ND de la Paix, 61 rue de Bruxelles, 5000 Namur, Belgium

Thierry Arnould

Laboratoire de Biochimie Cellulaire, Facultés Universitaires ND de la Paix, 61 rue de Bruxelles, 5000 Namur, Belgium

José Remacle

Laboratoire de Biochimie Cellulaire, Facultés Universitaires ND de la Paix, 61 rue de Bruxelles, 5000 Namur, Belgium

Blood stasis in leg veins is a situation commonly linked to the development of venous diseases such as varicoses. Such a stasis will provoke an ischemia, thus decreasing oxygen availability to tissues. Owing to its localization between blood and tissue, endothelium is the first target of this insult. The authors develop here a hypothesis in which the effect of oxygen deprivation on the functional state of the endothelium is the starting point of a cascade of events leading to the disorganization of the vessel wall typical of these pathologies. When venous human endothelial cells obtained from umbilical cords (HUVEC) are exposed to hypoxic conditions they become activated without change in their viability. The synthesis of a proinflammatory molecule (PAF, platelet-activating factor) and the adhesion of human polymorphonuclear neutrophils (PMN) on HUVEC are markedly increased during hypoxia incubation. These two processes are related to a calcium-dependent activation of endothelial cells due to a decrease of aden osine triphosphate (ATP) availability during hypoxia. Adherence of neutrophils to endothelial cells is the first step of diapedesis, which leads to the infiltration of these cells in the media of the veins, where they affect the smooth muscle cells and the connective tissue, leading to tissue alterations typical of the venous pa thologies. The authors propose that this sequential process which originates from a reduction in oxygen availability and which involves different cell types as one main cause of the venous disorders, in addition to genetic, hormonal, and mechanical factors.

Angiology, Vol. 44, No. 8, 639-646 (1993)
DOI: 10.1177/000331979304400808


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