Introduction
Platelets are small blood cells responsible for hemostasis (cessation of bleeding from the blood vessel) by binding to the vascular endothelium (inner lining of the blood vessels) and aggregating with the other platelets. This initiates the coagulation cascade (a series of steps during clot formation) and leads to fibrin mesh formation, thus preventing blood loss. Platelets are activated in response to the exposed thrombin, collagen, or other compounds due to tissue injury. Healthcare providers can monitor the platelet function by evaluating the bleeding time (time taken from the break of the vasculature to the formation of an effective platelet plug) and measuring platelet count. However, the function of platelets is not limited to clot formation, as they are also responsible for clot retraction through the action of certain activated receptors.
How Is a Clot Formed?
The existence of platelets and the concept of hemostatic function were developed during the 1800s, and the discovery of clotting factors began in the 1940s. There are around 13 major clotting factors that are expressed in Roman numerals. Blood clotting occurs when there is an injury or damage to the blood vessel. Platelets immediately adhere to the injured site and release certain chemicals, forming a platelet plug that stops external bleeding. The clotting factors make strands of blood-borne materials called fibrin that stick together and seal the wound. After a few days, the blood clot dissolves, and the injured site heals completely.
What Is Clot Retraction?
The phenomenon of clot retraction was first described in 1780 by William Hewson; since then, it has been a favorite subject of hematologists. A physiological process involving the contraction of the blood clot and oozing of the straw-colored fluid, serum, is called clot retraction. Clot retraction is mainly driven by the signaling of the platelet integrin (receptors that mediate the platelet adhesion process), resulting in the contraction of the fibrin mesh. The clot retraction study has been adopted as a simple approach to assess platelet function. The blood clot reduces in size or becomes smaller as the excess fluid extrudes (comes out) during the contraction of the fibrin clot. The contractile proteins such as actin, myosin, and thrombosthenin located in the cytoplasm of platelets are responsible for clot retraction.
What Is the Mechanism of Clot Retraction?
Clot retraction occurs due to the actomyosin-dependent contractile force (a force generated to facilitate contraction) of platelets bound to a fibrin mesh. It mainly occurs by shortening the fibrin fibers produced by the contraction of pseudopodia (attached platelet containing protein). Several studies have been conducted to understand or measure the force produced by a single thrombin-activated platelet bound to fibrinogen. Clot retraction was measured either based on the clot volume or platelet forces. After contact with the fibrinogen, the platelet begins to contract immediately, which was measured using cantilevers. Clot retraction changes the stiffness and organization of the blood clot. The adhesion strength and elasticity of the platelets are correlated, indicating that the exertion of more force by the platelet results in stiffer and more adhesive. Recent studies have demonstrated that the red blood cells in the clot assume a polyhedral shape, function to seal the clot and help in clot retraction.
Why Is Clot Retraction Necessary?
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Clot retraction is an important physiological mechanism necessary for the close contact of platelet cells during primary hemostasis, facilitating intercellular communication and platelet aggregation.
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Clot retraction brings the wound surfaces together, reduces the size of the wound, and promotes wound healing.
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The red blood cells form a polyhedrocyte barrier and seal the injured area, which helps prevent infection during wound healing.
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It helps to restore blood flow in case of thrombosis (formation of a blood clot within the blood vessels that causes complete or partial blockage).
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Various hematological disorders are associated with alterations in clot retraction. Failure of clot retraction can be seen in genetic diseases such as Glanzmann thrombasthenia (congenital bleeding disorder) and acquired diseases such as premature coronary artery disease (PCAD), bronchial asthma, ischemic stroke, uremia (accumulation of toxins in the blood), and other diseases.
How Is Clot Retraction Measured?
A clot retraction study measures the time the platelet plug takes to undergo retraction, which is the last step in blood coagulation. Clot retraction is a common phenomenon seen in clinical chemistry laboratories to determine the overall platelet function. The blood sample is drawn into the tube via a syringe without using anticoagulants to evaluate clot retraction. The specimens are set up in test tubes and observed under a camera. Photographs are taken initially and subsequently once every 30 minutes. The temperature is standardized, and the sample is left undisturbed. Each sample is normalized to a standard platelet count by mixing the patient’s platelet-poor plasma with the platelet-rich plasma. The clot retraction begins with the activation of platelets, followed by fibrin formation, and is long-lasting. Therefore, the effects of clot reduction are usually measured from ten minutes to several hours.
An alternate method followed is placing the platelet-rich plasma in a vial with a metal rod or a wooden stick and an agonist to initiate the clot formation. Following the clot formation, the clot and the rod are removed, and the amount of extruded serum is measured. A commercially available device called a thermodynamics analyzer system has been developed to continuously determine the clot area. The device has a light source and a cuvette; it measures light transmission and takes images every 15 seconds via a camera. This device helps to measure clot formation, fibrinolysis, thrombin generation, and clot retraction.
Conclusion
Clot retraction is a physiological process during which the blot clot reduces in size and draws the edges of the injured blood vessel by shortening the fibrin threads and squeezing out the excess serum. It depends on the release of multiple coagulation factors and is the last step of blood coagulation. Clot retraction is followed by fibrinolysis and tissue proliferation. Platelets play a vital role in this phenomenon by preventing excessive blood loss and infections at the injured site, thus promoting wound healing.
