Fats and Thrombus Formation

1961 ◽  
Vol 05 (03) ◽  
pp. 474-479 ◽  
Author(s):  
S.-E Bergentz ◽  
L.-E Gelin ◽  
C.-M Rudenstam
Keyword(s):  
Intravenous Administration ◽  
Blood Cells ◽  
Thrombus Formation ◽  
Clotting Time

Summary and conclusions1. Alimentary and intravenous administration of fat causes intravascular aggregation of blood cells and an increased tendency to formation of thrombi in ligated veins.2. This aggregation and thrombus formation after fat is completely prevented by heparin but is not influenced by the lengthening of clotting time induced by dicumarol.

Blood Flow Velocimetry in a Microchannel During Coagulation Using PIV and wOFV

2020 ◽  
Author(s):  
E. Kucukal ◽  
Y. Man ◽  
U. A. Gurkan ◽  
B. E. Schmidt
Keyword(s):  
Blood Flow ◽  
Blood Cells ◽  
Thrombus Formation ◽  
Blockage Ratio ◽  
Time Decay ◽  
Clotting Time ◽  
White Light Source ◽  
Flow Velocimetry ◽  
Flow Evolution ◽  
Time Decay Rate

Abstract This article describes novel measurements of the velocity of whole blood flow in a microchannel during coagulation. The blood is imaged volumetrically using a simple optical setup involving a white light source and a microscope camera. The images are processed using PIV and wavelet-based optical flow velocimetry (wOFV), both of which use images of individual blood cells as flow tracers. Measurements of several clinically relevant parameters such as the clotting time, decay rate, and blockage ratio are computed. The high-resolution wOFV results yield highly detailed information regarding thrombus formation and corresponding flow evolution that is the first of its kind.

Blood Flow Velocimetry in a Microchannel During Coagulation Using PIV and wOFV

2021 ◽  
Author(s):  
Erdem Kucukal ◽  
Yuncheng Man ◽  
Umut Gurkan ◽  
Bryan Schmidt
Keyword(s):  
Blood Flow ◽  
Blood Cells ◽  
Thrombus Formation ◽  
Blockage Ratio ◽  
Time Decay ◽  
Clotting Time ◽  
White Light Source ◽  
Flow Velocimetry ◽  
Flow Evolution ◽  
Time Decay Rate

Abstract This article describes novel measurements of the velocity of whole blood flow in a microchannel during coagulation. The blood is imaged volumetrically using a simple optical setup involving a white light source and a microscope camera. The images are processed using PIV and wavelet-based optical flow velocimetry (wOFV), both of which use images of individual blood cells as flow tracers. Measurements of several clinically relevant parameters such as the clotting time, decay rate, and blockage ratio are computed. The high-resolution wOFV results yield highly detailed information regarding thrombus formation and corresponding flow evolution that is the first of its kind.

Physico-Chemical Explanation of Blood Cell Adhesion in Thrombus Formation

1976 ◽  
Vol 36 (02) ◽  
pp. 430-440 ◽  
Author(s):  
A Marmur ◽  
E Ruckenstein ◽  
S. R Rakower
Keyword(s):  
Blood Cells ◽  
Thrombus Formation ◽  
Experimental Information ◽  
Deposition Surface ◽  
Physico Chemical ◽  
Quantitative Results ◽  
Energy Of Interaction ◽  
Induced Aggregation ◽  
Adhesion Of Platelets ◽  
Hydrodynamic Factors

SummaryA model is suggested which assumes that the rate of deposition of cells is determined both by hydrodynamic factors and by Brownian motion over the potential barrier caused by London and double-layer forces in the immediate vicinity of the deposition surface. The height of the barrier in the potential energy of interaction between blood cells and various surfaces is analyzed in relation to the physical properties of the cells, surfaces, and solutions. Based on this analysis, the adhesion of platelets to injured blood vessel walls and to non-biologic materials, the lack of adhesion of red blood cells under the same conditions, the mechanism of ADP induced aggregation and the interaction with blood flow are explained. The qualitative predictions of the model are substantiated by available experimental information. Quantitative results are presented in terms of a time constant, which typifies a period of contact with a surface, during which appreciable deposition occurs.

The Flowing Clotting Time (Thrombus Formation Time) a Sensitive Test of Hypercoagulability

1969 ◽  
Vol 21 (03) ◽  
pp. 516-523
Author(s):  
H Engelberg ◽  
L. P Engelberg
Keyword(s):  
Thrombus Formation ◽  
Formation Time ◽  
Sensitive Test ◽  
Clotting Time ◽  
Reliable Test ◽  
Time Test ◽  
Plasma Heparin

SummaryThe addition of small amounts of extrinsic thromboplastin or of thrombin to blood in vitro accelerated coagulation more frequently and to a greater extent when determined by the flowing time test than when measured by the silicone clotting time, or by the blood or plasma heparin tolerance tests. Similar results were obtained when intrinsic thromboplastin formation was stimulated by contact with glass. However there was little or no acceleration of the flowing clotting time of plasma obtained from aliquots of the thromboplastin-containing blood. These results indicate that the flowing clotting time (thrombus formation time) of whole blcod is a more reliable test of hypercoagulability than previously described blood or plasma clotting time tests.

Role of erythrocytes and platelets in the hypercoagulable status in polycythemia vera through phosphatidylserine exposure and microparticle generation

2013 ◽  
Vol 109 (06) ◽  
pp. 1025-1032 ◽  
Author(s):  
Chunyan Gao ◽  
Xue Yang ◽  
Jianan Li ◽  
Wei Wang ◽  
Jinxiao Hou ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Blood Cells ◽  
Significant Inhibition ◽  
Polycythaemia Vera ◽  
Factor V ◽  
Healthy Controls ◽  
Clotting Time ◽  
Thrombotic Risk ◽  
Few Data

SummaryThe development of thrombosis in polycythaemia vera (PV) involves multifactorial processes including pathological activation of blood cells. Release of microparticles (MPs) by activated cells in diseases is associated with thrombotic risk, but relatively few data are available in PV. The aim of the present study was to investigate the increase in MP release and exposure of phosphatidylserine (PS) on the outer membrane of MP-origin cells in patients with PV, and to analyse their procoagulant activity (PCA). PS-positive MPs and cells were detected by flow cytometry, while PCA was assessed with clotting time and purified coagulation complex assays. We found that PV patients had elevated circulating lactadherin+ MPs, which mostly originating from erythrocytes, platelets, granulocytes, and endothelial cells, as well as increased PS exposing erythrocytes/platelets as compared to secondary polycythaemia patients or healthy controls. These PS-bearing MPs and cells were highly procoagulant. Moreover, lactadherin competed factor V and VIII to PS and inhibited about 90% of the detected PCA in a dose-response manner while anti-TF antibody did no significant inhibition. Treatment with hydroxyurea is associated with a decrease in PS exposure and lactadherin+ MP release of erythrocytes/platelets. Our data demonstrate that PV patients are characterised by increased circulating procoagulant MPs and PS exposing erythrocytes/platelets, which could contribute to the hypercoagulable state in these patients.

2008 Sol Sherry Distinguished Lecture in Thrombosis—Platelet Adhesion in Acute Arterial Thrombosis

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Zaverio M. Ruggeri
Keyword(s):  
Vascular Injury ◽  
Blood Cells ◽  
Platelet Adhesion ◽  
Cancer Metastasis ◽  
Thrombus Formation ◽  
Arterial Occlusion ◽  
Vascular Wall ◽  
Membrane Receptors ◽  
Adhesive Properties ◽  
Vascular Integrity

Platelet adhesion is an essential function in response to vascular injury, through which single platelets bind to specific membrane receptors onto cellular and extracellular matrix constituents of the vessel wall and tissues initiating thrombus formation that arrests hemorrhage and permits wound healing. Pathological conditions that cause vascular alterations and blood flow disturbances may turn this defense process into a disease mechanism resulting in arterial occlusion, mostly in atherosclerotic vessels of the heart and brain. Besides their relevant role in hemostasis and thrombosis, platelet adhesive properties are central to a variety of pathophysiological processes that extend from inflammation to immune-mediated host defense and pathogenic mechanisms as well as cancer metastasis. All these activities depend on the ability of platelets to circulate in blood as sentinels of vascular integrity, adhere where alterations are detected, and signal the abnormality to other platelets and blood cells. In this respect, therefore, platelet adhesion to vascular wall structures, to one another (aggregation), or to other blood cells represents different aspects of the same fundamental biological process. Novel concepts and tools are being developed to advance our knowledge of the mechanisms through which platelets respond to vascular injury. Of particular interest are specific microparticles endowed with selective targeting properties conferred by recombinant adhesive domains that may be used for targeting areas of the vasculature with thrombogenic potential and for diagnostic purposes. Particles with such specific adhesive properties may also be used for the local delivery of anti-thrombotic drugs.

Effects of intravenous administration of a fat emulsion on blood coagulation in dogs

1959 ◽  
Vol 196 (5) ◽  
pp. 1015-1019 ◽  
Author(s):  
Harrison H. Shoulders ◽  
Robert C. Hartmann ◽  
H. C. Meng
Keyword(s):  
Blood Coagulation ◽  
Intravenous Administration ◽  
Intravenous Infusion ◽  
Bleeding Time ◽  
Plasma Fibrinogen ◽  
Fibrinogen Concentration ◽  
Clotting Time ◽  
Clot Retraction ◽  
Fat Emulsion ◽  
Abnormal Bleeding

A fat emulsion prepared for intravenous administration has been studied with regard to its effect upon blood coagulation in dogs. The most characteristic effects found during intravenous infusion of this material at a rate of 1 ml/min. were thrombocytopenia and marked shortening of clotting time. These effects were invariably observed in animals which had not previously received the emulsion. When subsequent infusions were given within 3 hours, no significant changes were observed. When the interval was extended to 1–13 days, variable responses occurred, at times characterized by pronounced hypocoagulability. If the repeat infusion was given 2 weeks or more after the initial one, the effects were similar to those observed during the first infusion. The prothrombin and thrombin clotting times and plasma fibrinogen concentration were not greatly altered during the infusion. Abnormal bleeding time, ‘prothrombin utilization’ and clot retraction accompanied the thrombocytopenia.

Changes in blood of dogs and rabbits by high fat intake

1959 ◽  
Vol 196 (3) ◽  
pp. 473-477 ◽  
Author(s):  
Roy L. Swank
Keyword(s):  
Surface Tension ◽  
Blood Cells ◽  
Buffy Coat ◽  
Sedimentation Rates ◽  
Fat Intake ◽  
Clotting Time ◽  
High Fat ◽  
Erythrocyte Sedimentation ◽  
Butter Fat ◽  
Erythrocyte Sedimentation Rates

The effect of large butter-fat meals on the blood of rabbits and dogs has been studied. Marked distortion of the red blood cells with adhesiveness and aggregation was observed. This was accompanied by slowing of the circulation and by changes in the surface tension of the plasma. In addition changes in the platelet counts, white blood counts, hematocrit and erythrocyte sedimentation rates were observed. Changes were also noted in the buffy coat, in the clotting time and in the nature of the clot.

scholarly journals Morphological Sequence of Spontaneously Forming Parietal Thrombi as Observed by Scanning Electron Microscopy (SEM)

1977 ◽  
Author(s):  
H.J. Genz ◽  
H. Metzger ◽  
P.F. Tauber ◽  
H. Ludwig
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Thrombus Formation ◽  
Shape Change ◽  
Inhibitory Effect ◽  
Endothelial Surface ◽  
Morphological Criteria ◽  
Fibrin Network ◽  
Tissue Specimens ◽  
Cellular Control

Spontaneous thrombus formation in human mesenteric veins was studied with the SEM. Tissue specimens were prepared according to Ludwig et al., Acta anatomica, 96, 469-477(1976). Platelet shape change, thrombus formation and organization and the morphological interactions between the various corpuscular elements of blood are demonstrated. The following morphological criteria of these processes are observed :(1) Platelets adhere to distinctly altered endothelial surfaces and exhibit pores in the membrane and pseudopodia. (2) Platelet aggregation and thrombus formation occur next to each other along the endothelial surface. Thrombi contain red blood cells and also a larger number of lymphocytes, but only a few platelets are hold prisoners within the fibrin network. Once caught in the mesh, such platelets do not show shape change compared to those being in contact with the endothelium. (3) Red blood cells between the thrombus fibers undergo form changes. Lymphocytes remain unaltered, but vice versa destroy adjacent fibrin fibers leading to partial loss of thrombus stability. This destruction occurs to a much lesser degree when platelets are near to the lymphocytes. It seems conceivable that platelets exert an inhibitory effect towards lymphocyte-induced fibrin proteolysis. The data suggest that both platelets and lymphocytes possibly represent a cellular control system that is responsible for the physiological clearance of spontaneously formed thrombi.

scholarly journals Red blood cells in thrombosis

Blood ◽  
2017 ◽  
Vol 130 (16) ◽  
pp. 1795-1799 ◽  
Author(s):  
James R. Byrnes ◽  
Alisa S. Wolberg
Keyword(s):  
Sickle Cell Disease ◽  
Venous Thrombosis ◽  
Red Blood Cells ◽  
Sickle Cell ◽  
Blood Cells ◽  
Thrombus Formation ◽  
Epidemiological Studies ◽  
Mechanistic Studies ◽  
Cell Disease ◽  
Growing Body

Abstract Red blood cells (RBCs) have historically been considered passive bystanders in thrombosis. However, clinical and epidemiological studies have associated quantitative and qualitative abnormalities in RBCs, including altered hematocrit, sickle cell disease, thalassemia, hemolytic anemias, and malaria, with both arterial and venous thrombosis. A growing body of mechanistic studies suggests that RBCs can promote thrombus formation and enhance thrombus stability. These findings suggest that RBCs may contribute to thrombosis pathophysiology and reveal potential strategies for therapeutically targeting RBCs to reduce thrombosis.

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