Related Experiment Video

Updated: Oct 2, 2026

Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
07:09

Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States

Published on: April 1, 2015

Blood viscosity, Raynaud's phenomenon and the effect of fibrinolytic enhancement

M L Ayres, P E Jarrett, N L Browse

    The British Journal of Surgery
    |January 1, 1981
    PubMed

    The whole blood and corrected blood viscosity of 17 patients with Raynaud's phenomenon (8 with idiopathic Raynaud's phenomenon and 9 with scleroderma-associated Raynaud's phenomenon) have been compared with 12 normal controls. Viscosity has been measured with a Contraves LSV1 rotating viscometer and the Wells-Brookfield microviscometer at 37 degrees C and 25 degrees C and shear rates ranging from 0.775 s-1 to 230 s-1. Blood viscosity was higher at both the lower temperature and the lower shear rates but this change was the same in the patients as in the normal subjects. There was a significantly higher level of plasma fibrinogen in the patients with scleroderma with a significant increase in the corrected blood viscosity, but not the whole blood viscosity, at both temperatures and all shear rates. The percentage increase of viscosity at low temperatures in the patients was the same as the controls. No evidence was found to substantiate the hypothesis that Raynaud's phenomenon is caused by an excessive increase of blood viscosity at low temperatures. Treatment of 10 patients with stanozolol, a stimulator of fibrinolysis, reduced the plasma fibrinogen and increased the haematocrit did not change the whole blood viscosity. Hand blood flow increased. The improvement of hand blood flow was not therefore caused by change in blood viscosity secondary to the reduction of plasma fibrinogen.

    More Related Videos

    Ferric Chloride-induced Murine Thrombosis Models10:37

    Ferric Chloride-induced Murine Thrombosis Models

    Published on: September 5, 2016

    Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization06:28

    Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization

    Published on: June 4, 2020

    Related Concept Videos

    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...
    Vascular Spasm01:16

    Vascular Spasm

    The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...
    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...
    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 forms a...
    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.
    Disorders of Hemostasis01:24

    Disorders of Hemostasis

    Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
    Thromboembolic Disorders
    Two factors primarily cause thromboembolic conditions.