Blood cell aggregation in thrombotic processes

by Haim I. Bicher

Publisher: C. C. Thomas in Springfield, Ill

Written in English
Published: Pages: 182 Downloads: 410
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  • Blood coagulation disorders.,
  • Thromboembolism.

Edition Notes

Bibliography: p. 132-176.

Statementby Haim I. Bicher.
SeriesAmerican lecture series, publication no. 835. A monograph in the Bannerstone division of American lectures in hematology
LC ClassificationsRC633 .B53
The Physical Object
Paginationx, 182 p.
Number of Pages182
ID Numbers
Open LibraryOL5471913M
ISBN 100398022321
LC Control Number73175068

Hemolytic uremic syndrome (HUS) is one of the disease processes that belong to thrombotic microangiopathies (TMAs). The common features for TMAs are microangiopathic hemolysis, thrombocytopenia, and thrombi in small vessels that lead to end organ damage. red blood cells lack CD46 52 it is well known that their activation and aggregation. Thrombotic thrombocytopenic purpura (TTP) is a blood disorder that results in blood clots forming in small blood vessels throughout the body. This results in a low platelet count, low red blood cells due to their breakdown, and often kidneys, heart, and brain dysfunction. Symptoms may include large bruises, fever, weakness, shortness of breath, confusion, and headache.   These observations suggest that AT [sub]1 R antagonists may retard the process of thrombus formation by inhibiting platelet aggregation. [sup][23] Our in vitro study indicates that the effect of Ang II on the expression of COX-2 was at least partially through the . Common Blood Thinners and Their Side Effects. Acetylsalycilic Acid (Aspirin, Ecotrin): the only over-the-counter blood thinner comes in regular strength and baby aspirin n has been around for a while. It inhibits platelet aggregation- meaning that it restricts the ability of the small cells that clump together to heal a wound from clumping together.

Hematologic measurements. Blood (10 ml) was with- drawn for platelet studies from the jugular cannula into a plastic syringe containing % sodium citrate as the an- ticoagulant (1:lO citrate/blood [volume/volume]). Blood was taken for platelet aggregation and whole blood cell. Platelet aggregation tests and blood pressure measurements were repeated after 8 weeks of therapy. Results: Systolic and diastolic blood pressure significantly decreased with losartan after 8 weeks (paggregation with ADP, collagen, and epinephrine (p>). The aggregation. Abstract We have previously shown that Endothelial Progenitor Cells (EPCs) bind and inhibit platelet function and impair thrombus formation, but the surrounding mechanisms that regulate this process have not been fully described. Herein, we addressed the mechanistic action of EPCs on platelet-thrombus formation and we highlighted the role of platelet P-selectin in this process.   Congenital thrombotic thrombocytopenic purpura: Lessons for recognition and management of rare syndromes. Pediatr Blood Cancer ; 5. Cermakova Z, Hrdlikova R, Sulakova T, Koristka M, Kovarova P, Hrachovinova I. Thrombotic thrombocytopenic purpura: incidence of congenital form of disease in north Moravia (region Moravia-Silesia).

Overview. Platelets, or thrombocytes, are the cells circulating in the blood that are involved in the cellular mechanisms of primary hemostasis leading to the formation of blood ction or low levels of platelets predisposes to bleeding, while high levels, although usually asymptomatic, may increase the risk of abnormality or disease of the platelets is called a.   The most important function of red blood cells (RBCs) is the carrying of oxygen, but they are also involved in inflammatory processes and during coagulation. RBCs are extremely deformable and elastic, as they are exposed to shear forces as they travel through the vascular system. In inflammatory conditions, and in the presence of hydroxyl radicals, RBCs loose their discoid shape.   It is not surprising that a hypercoagulable state occurs in the plasma in acute coronary syndromes, as indicated by blood prothrombotic markers or by the presence of new cardiovascular events in the face of powerful antithrombotic therapy [71–78].Inflammation can have a prothrombotic effect through the increase of tissue factor, platelet reactivity or acute phase reactant proteins such as. Human blood platelets, neutrophils, and vascular cells are known to play crucial roles in hemostatic, thrombotic, and inflammatory events in the human vascular system. Hellums and his colleagues have shown that the shear stress field associated with flow in blood vessels plays an important role in determining receptor expression and blood cell.

Blood cell aggregation in thrombotic processes by Haim I. Bicher Download PDF EPUB FB2

Additional Physical Format: Online version: Bicher, Haim I. Blood cell aggregation in thrombotic processes. Springfield, Ill., C.C. Thomas [] (OCoLC)   Blood sludging returns to our attention, as a major portion of Dr.

Bicher's review of blood cell aggregation. Certainly the early experimental work on circulating red cell aggregates in the forties and fifties has taken on a new significance, as a result of the recent interest in blood rheology and platelet aggregation, and should be reemphasized.

Author(s): Bicher,Haim I Title(s): Blood cell aggregation in thrombotic processes. Country of Publication: United States Publisher: Springfield, Ill., Thomas. The available data, including experimental studies, clearly indicate an excessive intravascular activation of circulating platelets in multiple sclerosis (MS) and their hyper-responsiveness to a variety of physiological activators.

Platelet activation is manifested as an increased adhesion and aggregation and is accompanied by the formation of pro-thrombotic microparticles.

Activated blood Cited by: 8. Blood coagulation and thrombin generation are primarily a function of platelets, coagulation factors, and endothelial cells. Red blood cells (RBCs) have generally been viewed as innocent bystanders in the clotting process. However, there has been a steadily growing clinical data revealing the active roles of erythrocytes in hemostasis.

RBCs may contribute to thrombosis in several Cited by: 1. Platelets are small cells in the blood that are responsible for clot formation at the site of bleeding. Platelets adhere to an injured site of the blood vessel and clump together in a process called aggregation, forming a platelet plug.

However, the same process may lead to thrombosis and blockage of blood flow in the vessel. Title: Understanding the Mechanism of Platelet Thrombus Formation under Blood Flow Conditions and the Effect of New Antiplatelet Agents VOLUME: 2 ISSUE: 1 Author(s):Shinya Goto Affiliation:Division of Cardiology, Department of Medicine Tokai University School of Medicine Shimokasuya, Isehara Kanagawa Japan.

Keywords:von willebrand factor, platelet, arterial thrombosis, shear. Red blood cell (RBC) aggregation induced by fibrinogen is a major determinant of the non-Newtonian flow behavior of human blood and has been suggested as a possible contributing factor for thrombogenesis.

Given the elevated fibrinogen levels and the high incidence of thrombotic accidents in nephrotic syndrome (NS), a study was designed to.

The editor has incorporated scientific contributions from a diverse group of leading researchers in the field of hematology and related blood cell research. This book aims to provide an overview of current knowledge pertaining to our understanding of hematology.

The main subject areas will include blood cell morphology and function, the pathophysiology and genetics of hematological. Blood cells circulate in a dynamic fluidic environment, and during hematologic processes such as hemostasis, thrombosis, and inflammation, blood cells interact biophysically with a myriad of vascular matrices—blood clots and the subendothelial matrix.

While it is known that adherent cells physiologically res Lab on a Chip Emerging Investigators Lab on a Chip Pioneers of Miniaturization. Thrombotic thrombocytopenic purpura (TTP) was first described by Moschowitz in Although it is now well recognised, being characterised by the classic pentad of fever, thrombocytopenia, microangiopathic haemolytic anaemia (MAHA), renal impairment, and fluctuating neurological signs, its precise pathophysiology remains elusive.

Several other syndromes including haemolytic uraemic. Title: Thrombotic Microangiopathy and Occult Neoplasia VOLUME: 10 ISSUE: 2 Author(s):Maria Teresa Pirrotta and Alessandro Bucalossi Affiliation:U.O. Oncologia, Ospedale pe, via Boccaccio,Empoli, Italy. Keywords:Thrombotic microangiopathies, occult malignancy Abstract: Thrombotic thrombocytopenic purpura (TTP), which is typically characterized by fever and central nervous system.

H.I. Bicher, Blood Cell Aggregation in Thrombotic Processes () C. Thomas Springfield J. Hardwire, J.R. Squire, The basis of the erythrocyte sedimentation rate Clin Sci () Lysophospatidic acid induced red blood cell aggregation in vitro.

Authors; RBCs (aggregation) exceeds a force of 25 p N. These results support (i) earlier data of a RBC associated component in thrombotic events under certain pathophysiological conditions and (ii) the concept to use RBCs in studies of cellular adhesion behavior, especially.

Purpose: The effects of antiplatelet and anticoagulant medications on the vasoocclusive and thrombotic complications of sickle cell disease are reviewed. Summary: Sickle cell disease is a chronic, inherited disorder characterized by chronic hemolytic anemia and vasoocclusive crisis.

Evidence suggests that circulating platelets in patients with sickle cell disease are chronically activated. The PRP obtained from human blood was washed with washing buffer, and the washed platelets (5 × 10 8 cells/mL) were suspended using buffer containing mM NaCl, mM KCl, 12 mM NaHCO 3, mM NaH 2 PO 4, mM glucose, mM MgCl 2, and % gelatin (pH ).

The platelets were then incubated with the insect extracts, followed by. Endothelial cells also express CD39, an enzyme that hydrolyzes ADP to AMP.

This process of ADP elimination prevents further pro-thrombotic platelet activation. In addition to CD39, endothelial cells express CD73, an enzyme that converts AMP to adenosine.

Background. Acquired thrombotic thrombocytopenic purpura (aTTP) is a rare, life‐threatening autoimmune thrombotic microangiopathy.

Current standard of care is therapeutic plasma exchange, immunosuppression, and caplacizumab, an anti‐von Willebrand factor nanobody, which is effective in treating aTTP episodes.

Effects of nattokinase, a pro-fibrinolytic enzyme, on red blood cell aggregation and whole blood viscosity February Clinical hemorheology and microcirculation 35() HTBT reviews applications involving basic and applied aspects of hemostasis, thrombosis, hematopoiesis, red blood cells, white blood cells, platelets, and transfusion.

Studies using cellular, biochemical, biophysical, immunological, genetic, pharmacological and molecular biological approaches to define normal and pathological processes are.

Abstract. Thrombotic thrombocytopenic purpura (TTP) and haemolytic-uraemic syndrome (HUS), are rare and poorly understood disorders involving multiorgan microvascular platelet thrombus formation and microangiopathic haemolytic anaemic (Kaplan et al, ; Kaplan ; White et al, ).Only in HUS has an initiating pathologic stimulus been identified in the form of toxins associated with.

Reduced red blood cell deformability and increased aggregation have been reported in such studies. 44 Yet, platelet activation was reduced. 45 6° head-down bedrest led to an increase in fibrinogen concentration without clinically relevant changes in blood coagulation capacity.

46 Thrombelastographic clotting times point rather towards an. Platelet aggregation was first recognized in the late s after a series of pioneering studies by Zahn (), Hayem (), Bizzozero ( and ), Osler (), and Eberth and Schimmelbusch ().

1–4,6 Using intravital imaging techniques, Bizzozero clearly established that small cell elements (in which he originated the term “Blut Plattchen” or blood platelets) clumped. The purpose of the study was to evaluate the direct effect of IS on thrombotic process.

We examined the impact of acute exposure to IS on thrombus development induced by electric current in Wistar. Platelet activation is manifested as an increased adhesion and aggregation and is accompanied by the formation of pro-thrombotic microparticles.

Activated blood platelets also show an expression of specific membrane receptors, synthesis many of biomediators, and generation of reactive oxygen species. The formation of a blood clot is a well-regulated process comprising three elements: (1) primary hemo-stasis, (2) secondary hemostasis/coagulation, and (3) fibrinolysis (Fig.

1) [Dahlback, ]. Primary he-mostasis is characterized by the adhesion, activation, and aggregation of platelets to. Bleeding and blood clotting, escape of blood from blood vessels into surrounding tissue and the process of coagulation through the action of platelets.

The evolution of high-pressure blood circulation in vertebrates has brought with it the risk of bleeding after injury to tissues. Mechanisms to. Sharma CP et al. Influence of L-ascorbic acid, blood cells and components on protein adsorption/desorption on polycarbonate.

Haemostasis. ;17() Pais E, Alexy T, Holsworth RE, Meiselman HJ. Effects of nattokinase, a pro-fibrinolytic enzyme, on red blood cell aggregation and whole blood viscosity. Clin. Hemorheol. Schistocytes should be evaluated on peripheral blood smears using an optical microscope at medium magnification and estimated as a percentage after counting at least red blood cells 2.

A schistocyte count should be requested and carried out when a diagnosis of thrombotic microangiopathies caused by red cell mechanical damage is suspected.

Ouared R, Chopard B. Lattice Boltzmann Simulations of Blood Flow: Non-Newtonian Rheology and Clotting Processes. J Stat Phys. ; Ref: ; Zhang JF, Johnson PC, Popel AS. Red blood cell aggregation and dissociation in shear flows simulated by lattice Boltzmann method.

Journal of Biomechanics. • ADAMTS13 is a protease that cleaves VWF in circulating blood and thereby limits platelet aggregation. Familial Thrombotic Thrombocytopenic Purpura = von Willebrand Factor-Cleaving Protease Deficiency = ADAMTS13 Deficiency • His ADAMTS13 gene sequencing shows homozygous splice site mutation, c+2T>C in ADAMTSThrombosis (from Ancient Greek θρόμβωσις thrómbōsis "clotting”) is the formation of a blood clot inside a blood vessel, obstructing the flow of blood through the circulatory a blood vessel (a vein or an artery) is injured, the body uses platelets (thrombocytes) and fibrin to form a blood clot to prevent blood loss.

Even when a blood vessel is not injured, blood clots.can improve red blood cell flexibility (deform-ability).6 7 In a 5-week double-blind place-bo-controlled study in 30 healthy subjects, g/day of omega-3 PUFAs as compared with g/day, significantly decreased plasma viscosity, red blood cell rigidity and systolic blood pressure.8 Thus, higher doses of marine omega-3 seem to be more effective.