Platelets coagulation and

Increases platelet coagulability and so activates platelet aggregation Connective tissue abnormalities... 

The allyl sulfur compounds of garlic also have an anticoagulant action (by inhibiting platelet coagulability) and inhibit cholesterol synthesis by inactivating HMG-CoA reductase. 

The allyl sulphur compounds (section 7.5.2.1) in garlic inhibit platelet coagulation, and again have a potentially beneficial effect with respect to thrombosis. 

Primary blood components iaclude plasma, red blood cells (erythrocytes), white blood cells (leukocytes), platelets (thrombocytes), and stem cells. Plasma consists of water dissolved proteias, ie, fibrinogen, albumins, and globulins coagulation factors and nutrients. The principal plasma-derived blood products are siagle-donor plasma (SDP), produced by sedimentation from whole blood donations fresh frozen plasma (FFP), collected both by apheresis and from whole blood collections cryoprecipitate, produced by cryoprecipitation of FFP albumin, collected through apheresis and coagulation factors, produced by fractionation from FFP and by apheresis (see Fractionation, blood-plasma fractionation). 

The calcium ion, necessary for blood-clot formation, stimulates release of bloodclotting factors from platelets (see Blood, coagulants and anticoagulants) (25). Neuromuscular excitabihty also depends on the relative concentrations of Na", Ca ", Mg ", and (26). Upon a decrease in... 

Plasma Inhibitors, In Vivo Anticoagulants. Fourteen naturally occurring compounds that normally exert an inhibiting effect on the activity of coagulation, platelet function, and fibrinolytic activity and complement systems have been identified within the circulating blood. 

Hemostasis is the cessation of bleeding from a cut or severed vessel, whereas thrombosis occurs when the endothelium lining blood vessels is damaged or removed (eg, upon rupmre of an atherosclerotic plaque). These processes encompass blood clotting (coagulation) and involve blood vessels, platelet aggregation, and plasma proteins that cause formation or dissolution of platelet aggregates. 

Describe the processes of hemostasis and thrombosis, including the role of the vascular endothelium, platelets, coagulation cascade, and thrombolytic proteins. 

Following endothelial injury, vessel-wall response involves vasoconstriction, platelet plug formation, coagulation, and fibrinolysis regulation. In normal circumstances, platelets circulate in the blood in an inactive form. After injury, platelets undergo activation, which consists of (1) adhesion to the subendothelium,... 

Platelets play a role in each of the mechanisms of normal hemostasis vasoconstriction, formation of the platelet plug, and blood coagulation. However, they are also involved in pathological processes that lead to atherosclerosis and thrombosis (formation of a blood clot within the vascular system). Antiplatelet drugs interfere with platelet function and are used to prevent the development of atherosclerosis and formation of arterial thrombi. 

For pH sensors used in in-vivo applications, especially those in continuous pH monitor or implantable applications, hemocompatibility is a key area of importance [150], The interaction of plasma proteins with sensor surface will affect sensor functions. Thrombus formation on the device surface due to accelerated coagulation, promoted by protein adsorption, provided platelet adhesion and activation. In addition, variation in the blood flow rate due to vasoconstriction (constriction of a blood vessel) and sensor attachment to vessel walls, known as wall effect , can cause significant errors during blood pH monitoring [50, 126],... 

Besides cholesterol efflux from arterial wall and its role in RCT, additional properties of HDL have been proposed for its protective anti-atherogenic activities. HDL protects vascular function by a number of potential alternative mechanisms, including inhibition of LDL oxidation [8,9], platelet aggregation and coagulation [10], and endothelial monocyte adhesion [11], as well as promotion of endothelial nitric oxide synthase (eNOS) [12], and prostacyclin synthesis [13-15]. The proposed alternate protective mechanisms for HDL are attractive but many of them lack validation under in vivo conditions. 

The rat carotid artery injured by a balloon catheter has been widely used as a model of angioplasty. The rat model is a proliferation model without foam cells (93). This form of injury causes immediate coagulation and thrombosis cascade in which platelets adhere, spread, and degranulate on the denuded surface of the artery, and approximately 24 hours later SMC begin to proliferate. Liposomal BPs, clodronate, and alendronate were injected to male sabra rats, 15 and 3mg/kg, respectively (52,69,76). Marked neointimal formation and decreased luminal area were observed in control animals. Neointima/media (N/M) ratio was 1.3 0.2, and luminal stenosis was 44 3%. LC and LA suppressed intimal growth when administered intravenously on day -1 and day 6. N/M ratios were reduced by 60% and 69% for LC and LA, respectively. 

Hematologic effects Thrombocytopenia, inhibition of the secondary phase of platelet aggregation, and abnormal coagulation parameters have occurred determine platelet counts and bleeding time before initiating therapy, at periodic intervals, and prior to surgery. 

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