Platelet activation aggregation

The intetaction of thrombin with platelets causes increases in cytoplasnic Ca shape change and the conversion of prothrombin to thrombin via the prothrombinase complex leading to further platelet activation, aggregation and secretion. The concentration of free a-thrombin in plasma following ph)Tsiological activation has been determined to be in the range of O.S-2nM due to... 

Thrombosis (platelet activation, aggregation, and deposition at the vascular injury site)... 

Platelet activating factor (PAF) was first identified by its ability (at low levels) to cause platelet aggregation and dilation of blood vessels, but it is now known to be a potent mediator in inflammation, allergic responses, and shock. PAF effects are observed at tissue concentrations as low as 10 M. PAF causes a dramatic inflammation of air passages and induces asthma-like symptoms in laboratory animals. Toxic-shock syndrome occurs when fragments of destroyed bacteria act as toxins and induce the synthesis of PAF. This results in a drop in blood pressure and a reduced... 

An imidazoquinazoline constitutes still another compound that does not fall in the classification of a nonsteroid antiinflammatory agent yet shows good platelet anti aggregating activity. Condensation of benzyl chloride 128 with the ethyl ester of glycine gives alkylated product... 

The formation of a platelet aggregate requires the recruitment of additional platelets from the blood stream to the injured vessel wall. This process is executed through a variety of diffusible mediators which act through G-protein-coupled receptors. The main mediators involved in this process are adenosine diphosphate (ADP), thromboxane A2 (TXA2), and thrombin (factor Ila). These mediators of the second phase of platelet activation are formed in different ways. While ADP is secreted from platelets by exocytosis, the release of TXA2 follows its new formation in activated platelets. Thrombin can be formed on the surface of activated platelets (see Fig. 2). 

Most antiplatelet dtugs only partially inhibit platelet activation. In contrast, blockers of GPIIb/llla interfere at the end of the pathway common to platelet aggregation. They prevent fibrinogen and vWf from... 

Platelet-activating Factor Platelet Aggregation Inhibitors Platelet-derived Growth Factor Receptor Platelet Inhibitors Platelets... 

Thrombin and other agents cause platelet aggregation, which involves a variety of biochemical and morphologic events. Stimulation of phosphofipase C and the polyphosphoinositide pathway is a key event in platelet activation, but other processes are also involved. 

Administration of clopidogrel is recommended for all patients with STE ACS (Table 5—2).3 Clopidogrel blocks adenosine diphosphate receptors on platelets, preventing the expression of glycoprotein Ilb/IIIa receptors and thus platelet activation and aggregation. 

Platelet-activating factor A mediator of platelet aggregation and inflammation that is produced in response to stimuli, such as white blood cells. 

Human platelets Platelet activation and aggregation by inducing Ca2+ influx [112]... 

Fig. 9.1. A dysfunctional or injured endothelium is at the basis for initiation of and progression to atherosclerosis. Several mechanisms, such as adhesion molecules or liberation of von Willebrand factor (vWf, upper panel), determine a series of phenomena, including platelet activation and aggregation. This participation of platelets involves the implication of molecules like glycoprotein Ilb/IIIa, fibrinogen, and von Willebrand factor. The endothelium also acts as a source of signals that regulate local functions, including VSMCs (lower panel). A list of the most relevant messengers produced by a functional and a dysfunctonal endothelium is presented in the lower panel...

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