#PLASH KO ENGLISH MEIN KYA KAHATE HAIN ACTIVATOR#
Endothelial-ADPase degrades the platelet activator ADP. The intact endothelial lining inhibits platelet activation by producing nitric oxide, endothelial- ADPase, and PGI 2 (prostacyclin). From left to right: human erythrocyte, activated platelet, leukocyte. Scanning electron micrograph of blood cells. More accurate biophysical models of the platelet surface morphology, which model its shape from first principles, make it possible to obtain a more realistic platelet geometry in a calm and activated state.
This approximation is often used to model the hydrodynamic and optical properties of a platelet population, as well as to restore the geometric parameters of individual measured platelets by flow cytometry. In a first approximation, the platelet shape can be considered similar to oblate spheroids, with a semiaxis ratio of 2 to 8. Activated platelets have cell membrane projections covering their surface.
This dense tubular system is connected to the surface platelet membrane to aid thromboxane A2 release.Ĭirculating inactivated platelets are biconvex discoid (lens-shaped) structures, : 117–18 2–3 µm in greatest diameter. Membranous zone – contains membranes derived from megakaryocyte smooth endoplasmic reticulum organized into a dense tubular system which is responsible for thromboxane A2 synthesis.Delta granules, or dense bodies, contain ADP, calcium and serotonin, which are platelet-activating mediators. Alpha granules contain clotting mediators such as factor V, factor VIII, fibrinogen, fibronectin, platelet-derived growth factor, and chemotactic agents. Organelle zone – is rich in platelet granules.Sol-gel zone – is rich in microtubules and microfilaments, allowing the platelets to maintain their discoid shape.Peripheral zone – is rich in glycoproteins required for platelet adhesion, activation and aggregation.Structurally the platelet can be divided into four zones, from peripheral to innermost: Platelets also participate in both innate and adaptive intravascular immune responses. Some would add the subsequent retraction and platelet inhibition as fourth and fifth steps to the completion of the process and still others would add a sixth step, wound repair. These processes may overlap: the spectrum is from a predominantly platelet plug, or "white clot" to a predominantly fibrin, or "red clot" or the more typical mixture. Formation of this platelet plug (primary hemostasis) is associated with activation of the coagulation cascade, with resultant fibrin deposition and linking (secondary hemostasis). Third, they connect to each other through receptor bridges: aggregation. Second, they change shape, turn on receptors and secrete chemical messengers: activation. First, platelets attach to substances outside the interrupted endothelium: adhesion. They gather at the site and, unless the interruption is physically too large, they plug the hole. One major function of platelets is to contribute to hemostasis: the process of stopping bleeding at the site of interrupted endothelium. The platelets congregate around the wound in order to create a cap to stop blood flow out of the tissue. As more platelets gather around the opening, they produce more ligands to amplify the response.
The ligands, denoted by letter L, signal for platelets (P) to migrate towards the wound (Site A).
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