The vascular system prevents bleeding through vessel contraction, diversion of blood flow from damaged vessels, initiation of contact activation of platelets with aggregation, and contact activation of the coagulation system.4 The vessel wall contains varying amounts of fibrous tissue such as collagen and elastin, as well as smooth muscle cells and fibroblasts. Arteries are the vessels that take blood away from the heart and have the thickest walls of the vascular system. Veins return blood to the heart, and are larger with a more irregular lumen than the arteries. Veins, however, are thin walled, with elastic fibers found only in larger veins. Arterioles are a smaller subdivision of arteries, and venules are smaller subdivisions of veins. Capillaries are the thinnest walled and most numerous of the blood vessels. They are composed of only one cell layer of endothelium that permits a rapid rate of transport materials between blood and tissue.5
The process in which coagulation occurs begins with injury to a vessel. The first response of a cut vessel is vasoconstriction or narrowing of the lumen of the arte-rioles to minimize the flow of blood from the wound site. The blood is ordinarily exposed to only the endothelial cell lining of the vasculature. When this is invaded, the exposed deeper layers of the blood vessel become targets for cellular and plasma components. Vasoconstriction occurs immediately and lasts a short period of time. It allows for increased contact between the damaged vessel wall, blood platelets, and coagulation factors. Vasoconstriction is caused by several regulatory molecules including serotonin and thromboxane A2, which interacts with receptors on the surface of cells of the blood vessel wall. These are products of platelet activation and endothelium. Endothelial cells lining the lumen of the blood vessel are the principal elements regulating vascular functions. Physiologically, the surface of endothelial cells is negatively charged and repels circulating proteins and platelets, which are negatively charged.6 Vasoconstriction occurs very quickly and is effective in stopping bleeding in small blood vessels but cannot prevent bleeding in larger vessels. Other systems are required for this task.
The endothelium contains connective tissue such as collagen and elastin. This matrix regulates the permeability of the inner vessel wall and provides the principal stimuli to thrombosis following injury to a blood vessel. Circulating platelets recognize and bind to insoluble subendothelial connective tissue molecules. This process is dependent on molecules that are in plasma and on platelets. Two factors, von Willebrand (vWF) and fibrinogen, participate in the formation of the platelet plug and the insoluble protein clot, resulting in the activation of the coagulation proteins. Receptor molecules not only adhere to platelets and damaged vessel components but also allow platelets to use vWF and fibrinogen to bind platelets and form a plug. Blood flows out through the wall and comes in contact with collagen. Collagen is an insoluble fibrous protein that accounts for much of the body's connective tissue. Vessel injury leads to the stimulation of platelets. Platelets contain more of the contractile protein actomyosin than any cells, other than muscle cells, giving them the ability to contract. Basically platelets adhere to collagen and other platelets adhere to them. A plug is built and the platelets' ability to further contract compacts the mass.7
In forming the initial plug, platelets have now built a template on a lipoprotein surface, which in turn activates tissue factor. The balance between coagulation proteins and anticoagulants now leans toward coagulation. This process will accelerate vasoconstriction, platelet plug development, and the formation of cross-linked fibrin clot (Fig. 15.1).
Events Following Vascular Injury
1. Thromboresistant properties of a blood vessel maintain blood in a fluid state.
2. After vascular injury, subendothelial components of collagen induce platelet aggregation, which is mediated by vWF and platelet receptor glycoprotein Ib.
3. Further platelet recruitment occurs as a result from fibrinogen binding to its platelet receptor, glycoprotein IIb/IIIa.
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