Prostacycline

The term "Prostacycline (PGI)" is a collective term for bicyclic prostaglandins.

PGI2 is the most effective thrombocyte aggregation inhibitor. PGI2 is an antagonist of the thrombboxanes, thus an inhibitor of clotting, which is formed by the endothelium. Its formation is stimulated by thrombin and noradrenalin. Prostacyclins inhibit the adhesion and aggregation of the thrombocytes. They have a vasodilatory effect.

The endothelium is a highly complex organ which, in addition to its aggregatory and antiaggregatory function, also plays a major role in wound healing. By secreting cytokines, e.g. the "stroma-cell-derived factor-1", it recruits precursors of leukocytes from the blood, which contribute to the healing of injured vessels.

Closely intertwined with the coagulation system are the inflammatory processes and the immune response. This interdependence manifests itself in the form of disorders of the coagulation system in severe infarcts, such as consumption coagulation, sepsis, polytrauma or pancreatitis. Particularly involved is the endothelium of one of the organs, where inflammatory processes manifest themselves very early, as leukocytes are deposited in the vessels and surrounding tissue during inflammation. They were previously bound to the endothelium with the help of selectins and by means of special adhesion molecules (ICAM). By secretion of proteases from the leukocytes, the endothelia are actively destroyed during this adhesion process, whereby the leukocytes can then migrate further into the surrounding tissue.

Such inflammatory processes and the complex cytokine activations play a decisive role in the development of arteriosclerosis and its secondary diseases. A large number of cytokines and other mediators have already been identified.

Lipoprotein A plays an important role in the development of arteriosclerosis. Among other functions that the lipoprotein performs, the following effects are important for coagulation:

• Increase of PAI-1 expression in the endothelium

• Inhibition of plasma activity by inhibition of t-PA synthesis

• Inhibition of the formation of plasmin on the endothelial surface

• activation of the beta-transforming growth factor and thus further inhibition of fibrinolysis and

• Acceleration of the growth of vascular smooth muscle cells

This inhibits fibrinolysis, which antagonises the coagulation process, in its course.

1. HA Neumann (2014) The coagulation system. ABW-Scientific Publisher GmbH Berlin