Blood platelet aggregation, preventing

Dipyridamole exerts its effect by inhibition of platelet phosphodiesterase E5, increasing cyclic guanosine monophosphate and cyclic adenosine monophosphate (cAMP). By inhibiting its uptake and metabolism by erythrocytes, dipyridamole also increases the availability of adenosine within blood vessels, promoting inhibition of platelet aggregation and local vasodilatation. " Dipyridamole may also inhibit cAMP phosphodiesterase in platelets, which further increases cAMP levels and may enhance endothelial nitric oxide production, contributing to its antithrombotic effect. Existing trials of dipyridamole in stroke have focused on secondary prevention and will be discussed briefly. 

B-NOD is a new NO donor compound. It has a chemical NO-releasing group similar to that of NTG, however, it releases NO in vitro and in vivo. After administration of B-NOD in vivo its activity persists for more than 7 h. In vitro, the release of NO from B-NOD was augmented by the presence ofliving cells (blood platelets). B-NOD increased cGMP levels and prevented thrombin-induced platelet aggregation in vitro in the same manner as SNP. In vivo, administration of B-NOD in rabbits did not cause a fall in blood pressure or an increase in heart rate [97]. 

Many studies have shown that ginseng has a protective effect on the development of atherosclerosis that may lead to myocardial infarction and other cardiovascular diseases. The preventive effects on cardiovascular diseases of ginseng include its potential antihypertensive and antiatherosclerotic effects. Ginsenosides are likely to be responsible for some of these effects as they have been shown to have inhibitory effects on platelet aggregation and to suppress thrombin formation as well as an effect on blood vessel contraction. 

Effect on blood Platelets are the important factors in thrombus formation and aspirin has been shown to inhibit platelet aggregation. They reduce the blood prothrombin level by inhibition of prothrombin synthesis and prothrombin time is prolonged. The aspirin suppresses the synthesis of thromboxane (TXA ) in the platelets. They also prolong the bleeding time due to prevention of platelet aggregation which may be due to inhibition of release of adenosine diphosphate (ADP) from the platelets by salicylates. 

As regards the function of this electronegative shield in some cell-types, membrane sialic acids prevent aggregation due to electrostatic repulsion in, for example, blood platelets, erythrocytes, and carcinoma cells in culture,418 whereas, in others, for example, chick, embryonic muscle-cells,422 aggregation is facilitated, most probably by Ca24 bridges. Sialic acid was also shown to be involved in the attachment both of endothelium and epithelium to glomerular basement-membranes of rat kidney.423... 

A significant body of evidence suggests that the calcium channel blockers may interfere with platelet aggregation in vitro and prevent or attenuate the development of atheromatous lesions in animals. Clinical studies have not established their role in human blood clotting and atherosclerosis. 

Thrombus Formation. The thromboxanes, especially TXA2, cause platelet aggregations that result in blood clot formation.73 It is unclear whether excessive thrombus formation (as in deep vein thrombosis or coronary artery occlusion) is initiated by abnormal thromboxane production. Certainly, inhibition of thromboxane synthesis will help prevent platelet-induced thrombus formation in individuals who are prone to specific types of excessive blood clotting.84... 

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