Studii recente acorda o atentie deosebita structurii si mai ales functiei endoteliului venos in reglarea fenomenelor de tromboza si rolului jucat de acesta in insuficienta venoasa cronica (IVC).

In lucrare sunt mentionati principalii factori produsi la nivel endotelial, cu rol cert sau posibil in declansarea modificarilor trofice din IVC. Insistam asupra interleukinei 1 (IL-1), citokina proinflamatoare produsa atat de leucocitele atasate endoteliului, cat si de celulele endoteliale activate in urma aderarii acestora. IL-1 stimuleaza adeziunea leucocitelor la celulele endoteliale prin inductia de ELAM-1 (endothelial leukocytes adhesive molecules) si NCAM-1 (netrophil cells adhesive molecules). De asemenea, stimuleaza eliberarea de factori de coagulare de catre endoteliul venos si reduce activitatea fibrinolitica.

Autorii isi propun sa studieze IL-1 in diferite forme clinice de insuficienta venoasa cronica, prin metode imuno-histochimice.

Recent studies grant an exquisite attention to the role of the structure and, mainly the function of the venous endothelium, regarding the trombosis regulation and the pathogenesis of the chronic venous insufficiency (CVI).

This paper presents the main factors synthesized by the endothelium, and having a certain or feasible trigger role in the trophic changes of CVI.

We focus on IL-1, a proinflammatory cytokin released both by the leuyocytes attached to the leukocytes attached to the endothelium and by the endothelial cells, activated by the leukocyte adherence.

IL-1 stimulates the adhesion of the leukocytes to the endothelial cells by the induction of ELAM-1 (endothelial leukocytes adhesive molecules), ICAM-1 (inter cells adhesive molecules) and NCAM-1 (netrophil cells adhesive molecules). IL-1 enhances the release of the coagulation factors from the venous endothelium and decreases the fibrinolytic activity.

The authors aim to study IL-1 in different forms of chronic venous insuffiency, using immunohistochemical methods.