Pathophysiology of Thrombus formation
Thrombus formation and propagation depends on the presence of Virchow's triada

Circulatory stasis

Hypercoagulable state

Endothelial Injury

Blood Homeostasis

Although nitric oxide has been known about for a long time, its biological significance was discovered only recently. By 1987 it was shown that nitric oxide is released by the endothelial cells lining blood vessels (Palmer et al, 1987). From here the nitric oxide diffuses to adjacent smooth muscle cells in the vessel wall and causes them to relax, allowing vasodilation. Nitric oxide is now regarded as a key endothelium-derived mediator (Messenger) that plays important role in vascular homeostasis and in controlling the blood pressure and local blood flow.

To mark the significance of the work on nitric oxide, the 1998 Nobel Prize for physiology or medicine was awarded to Furchgott, Ignarro, and Murad.

Nitric oxide (NO) is produced in the body by vascular endothelium and smooth muscle, cardiac muscle, and many other cell types. The substrate for NO is L-arginine that is transported into the cell. When acted upon by Nitric-Oxide-Synthase (NOS) enzyme, NO and citrulline are formed.

NO has the following functions:

1. Vasodilation
2. Inhibition of vasoconstrictor influences.
3. Inhibition of platelet adhesion to the vascular endothelium (Anti-thrombotic Function)
4. Inhibition of leukocyte adhesion to vascular endothelium (Anti-inflammatory Function)
5. Antiproliferative (e.g., inhibits smooth muscle hyperplasia following vascular injury)

When Nitric oxide (NO) production is impaired as occurs when the vascular endothelium becomes damaged or dysfunctional, the following can result:

1. Vasoconstriction and stenosis
2. Platelet aggregation and adhesion leading to thrombosis
3. Upregulation of leukocyte and endothelial adhesion molecules leading to enhanced inflammation
4. Increased inflammation and tissue damage mediated by reactive oxygen species such as superoxide anion and hydroxyl radical  
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