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Platelet Zones

1. The peripheral zone is associated with platelet adhesion and aggregation.

2. The sol gel zone provides a cytoskeletal system for platelets and contact when the platelets are stimulated.

3. The organelle zone contains three types of granules: alpha, dense bodies, and lysosomes.

4. The membrane system contains a dense tubular system in which the enzymatic system for the production of prostaglandin synthesis is found.

1. The peripheral zone is associated with platelet adhesion and aggregation.

2. The sol gel zone provides a cytoskeletal system for platelets and contact when the platelets are stimulated.

3. The organelle zone contains three types of granules: alpha, dense bodies, and lysosomes.

4. The membrane system contains a dense tubular system in which the enzymatic system for the production of prostaglandin synthesis is found.

disc to spiny spheres. Glycoprotein (GP) Ib and vWF aid in adhesion. This is primary aggregation and is reversible. This reaction is mediated by the release of platelet granules.

• REACTION 2 (AGGREGATION): In response to chemical changes, these events lead to platelet aggregation in which platelets adhere to other platelets. Platelet shape change occurs.

• REACTION 3 (RELEASE): Platelets release the contents of their dense granules. The release of these granules constitutes a secondary aggregation that is irreversible. Thromboxane A2 is released by platelets, which promotes vasoconstriction. ADP amplifies the process.

• REACTION 4 (STABILIZATION OF THE CLOT): This reaction is responsible for thrombus formation. The adherent and aggregated platelets release factor V and expose platelet factor 3 to accelerate the coagulation cascade and promote activation of clotting factors and ultimately stabilize the platelet plug with a fibrin clot.

The platelet membrane contains important receptors called GPs on the platelet surface. Further interactions are mediated by both plasma protein receptors of vWF and fibrinogen. Other activators of platelets are thrombin, ADP, thromboxane A2, serotonin, epinephrine, and arachidonic acid.

The receptor for vWF is GPIb-IX. GPIIb/IIIa are receptors for fibronectin, vWF, fibrinogen, and factors V and VIII. This interaction recruits more platelets to interact with each other.11 Adhesion of platelets to collagen and each other can occur without contraction or shape change. Contraction causes shape change into a spiny sphere. Exposure of a negatively charged membrane leads to secretion of granular contents. These activated platelets release ADP and synthesized thromboxane A2, which mediate activation of additional platelets, resulting in the formation of a platelet plug.12

Platelet Aggregation Principle

Aggregation defines the ability of platelets to stick to one another. The formation of aggregates is observed with a platelet aggregometer. This is a photo-optical instrument connected to a chart recorder. Light trans-mittance through the sample is increased and converted into electronic signals, which are amplified and recorded. A characteristic curve is formed with each aggregating agent. Primary aggregation is the first wave of aggregation and is preceded by a shape change except when platelets are stimulated with epinephrine (Fig. 15.4). Primary aggregation is a reversible process. The second phase of platelet aggregation occurs when platelet granule contents are secreted. Secondary aggregation is irreversible. Epinephrine, collagen, ADP, and arachidonic acid are the aggregating agents most frequently used in clinical platelet aggregation.

1. Epinephrine (EPI): When added to platelet rich plasma (PRP), it will stimulate platelets to aggregate. Normal platelets will respond by releasing endogenous ADP from their granules. Both primary and secondary aggregation is seen. An abnormal response is due to an absent or decreased release of nucleotides from dense granules.

2. Adenosine diphosphate (ADP): When added to PRP, it will stimulate platelets to change their shape and aggregate. Aggregation is induced by exogenous ADP at a high dose of 20 pmol/L. The primary and secondary wave aggregations are indistinguishable. Reversible aggregation may occur due to an inadequate

Platelet Aggregation Tracings

Platelet Aggregation Tracings

Figure 15.4 Platelet aggregation. Note the stages of aggregation, which include primary and secondary aggregation as well as shape change and plug formation.

release of nucleotides. Lack of a secondary wave is indicative of defective thromboxane production and/or a defective granule pool.

3. Collagen: When added to PRP, the platelets adhere to the collagen, followed by shape change, release of endogenous ADP, and then aggregation. An abnormal response to collagen may be seen if thromboxane production is deficient. Aggregation is slower and less complex, resulting in a decreased response.

4. Arachidonic acid (AA): This is a fatty acid present in membranes of human platelets and liberated from phospholipids. In the presence of the enzyme cyclooxygenase, oxygen is incorporated to form the endoperoxide prostaglandin G2 (PGG2). PGG2 is then converted to thromboxane A2, a potent inducer of platelet aggregation.

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