Pathophysiological aspects of platelet aggregation in relation to blood flow rheology in microcirculation.
Platelet aggregates play an important role in rheology of the blood flow in microcirculation. The formation of platelet aggregates markedly raise the threshold diameter of the vessel at which the inversion of Fahraeus-Lindquist effect takes place. In different diseases (ischemic heart disease, diabetes) thromboxane A2 production by platelets is increased and, as a consequence, platelet aggregate formation is facilitated. Platelet aggregation is modulated by several mechanisms, among which thromboxane A2 and thrombin increase and prostacyclin decrease formation of platelet aggregates. Prostacyclin is able also to increase blood red cells deformability thus it appears one of the most important factors for the control of blood flow rheology in microcirculation. However, prostacyclin production is limited in time, and repeated and close periods of venous stasis induce exhaustion of prostacyclin production and increase the formation of platelet aggregates.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D001790:Blood Physiological Phenomena; D001792:Blood Platelets / Q000378:metabolism; D001809:Blood Viscosity / Q000187:drug effects; D011464:Epoprostenol / Q000096:biosynthesis; D004912:Erythrocytes / Q000502:physiology; D006801:Humans; D007511:Ischemia / Q000503:physiopathology; D008833:Microcirculation / Q000502:physiology*; D010974:Platelet Aggregation / Q000187:drug effects; D012212:Rheology; D013928:Thromboxane A2 / Q000096:biosynthesis / Q000494:pharmacology
D013928:Thromboxane A2; D000244:Adenosine Diphosphate; D011464:Epoprostenol