Related Experiment Video

Updated: Mar 5, 2026

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
08:30

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation

Published on: August 14, 2017

11.9K

Release of beta-lysin from platelets by thrombin and by a factor produced in heparinized blood

J G Tew, R R Roberts, D M Donaldson

    Infection and Immunity
    |January 1, 1974
    PubMed

    Removal of calcium by either citrate, oxalate, or ethylenediaminetetraacetate inhibited coagulation of blood at an early stage and prevented the release of beta-lysin from platelets. In contrast, heparin caused platelet agglutination and stimulated beta-lysin release in vitro and in vivo. This release was calcium dependent and may have been due to a calcium-dependent reaction in the blood coagulation sequence. Thrombin which by-passed the early calcium-dependent stages of coagulation directly stimulated the release of beta-lysin from platelets. However, thrombin alone or in combination with other plasma factors was not as effective in releasing beta-lysin as the regular coagulation process. Thrombin's platelet degranulating activity correlated with its beta-lysin releasing activity. In contrast to thrombin, staphylococcal coagulase, which also by-passed the calcium-dependent stages of coagulation, coagulated citrated blood without releasing beta-lysin. The release of beta-lysin has been observed previously in the absence of blood coagulation, but this is the first observation of coagulation without beta-lysin release. It is clear that beta-lysin is released from platelets during coagulation by the direct action of thrombin and that it may be released in an earlier calcium-dependent reaction.

    More Related Videos

    A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time09:38

    A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

    Published on: February 14, 2017

    14.5K
    Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay13:08

    Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

    Published on: September 9, 2012

    19.5K

    Related Concept Videos

    Extrinsic and Intrinsic Pathways of Hemostasis01:20

    Extrinsic and Intrinsic Pathways of Hemostasis

    Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
    The Extrinsic Pathway
    The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
    14.3K
    Formation of the Platelet Plug01:22

    Formation of the Platelet Plug

    The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
    As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
    10.2K
    Clot Retraction and Fibrinolysis01:16

    Clot Retraction and Fibrinolysis

    After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
    9.7K
    Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

    Anticoagulant Drugs: Low-Molecular-Weight Heparins

    Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
    2.2K
    Introduction to Hemostasis01:05

    Introduction to Hemostasis

    Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
    The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized,...
    15.5K
    Structure and Function of Platelets01:18

    Structure and Function of Platelets

    The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
    Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000...
    4.2K