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Effects of Antithrombotic and Results of Drug Screening
Published in Josef Hladovec, Antithrombotic Drugs in Thrombosis Models, 2020
The fact that an increased level of catecholamines in the blood may somehow be related to the thrombotic tendency has been known for a long time. It obviously reflects the survival value of a functional increase in hemostatic capacity under stressful situations. At the same time, the targets of the catecholamine effect may be manifold: Vasoconstriction in special circulation areas together with the inotropic effect on the myocardium leading to hemodynamic changes and blood flow redistribution.Direct injurious effects on the vascular wall, particularly endothelium.Effects on blood clotting, fibrinolysis, and platelets.Metabolic effects (lipomobilization, glycogenolysis, gluconeogenesis, etc.).
Application of Bioresponsive Polymers in Drug Delivery
Published in Deepa H. Patel, Bioresponsive Polymers, 2020
Manisha Lalan, Deepti Jani, Pratiksha Trivedi, Deepa H. Patel
Zhang et al. developed a thrombin responsive system for heparin delivery in the management of coagulation disorders. Heparin was coupled to HA through a thrombin-cleavage peptide. The microneedles released heparin in response to increased thrombin from the blood clots. Such a system promises to be utility in the management of abnormal blood clotting and acute pulmonary thromboembolism [24].
The Hematologic System and its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Hemophilia is actually a group of diseases, each caused by a lack of a different coagulation factor. Each has slightly unique characteristics, but ail involve a deficiency in the platelet-mediated clotting mechanism. The missing factors, however, are not necessary for the tissue thromboplastin mechanism for initiating blood clotting. So clotting occurs almost normally if the tissues are torn severely enough to form adequate thromboplastin. A simple rupture without much local tearing, however, causes bleeding that can last for hours.
Hemostasis-on-a-chip / incorporating the endothelium in microfluidic models of bleeding
Published in Platelets, 2023
Yumiko Sakurai, Elaissa T. Hardy, Wilbur A. Lam
Bleeding disorders (i.e. hemophilia and von Willebrand disease) affect hemostasis, and affected patients may exhibit various degrees of bleeding problems. Historically, patients with a suspected bleeding disorder underwent a “bleeding time test” to directly assess the patient’s bleeding risk. This test includes small incisions on the patient’s arm and recording the time when the bleeding stops [1] but the procedure is difficult to control and is invasive. Currently, the bleeding time test has largely been replaced by assays using blood collected through a venipuncture, assessing the risks of abnormal bleeding and blood clotting. Specifically, the assays include prothrombin and partial thromboplastin time, platelet function assays, and various viscoelastic tests. The assays can be performed as point-of-care in clinical settings [2–4] where timely assessment is needed in the emergency department, surgery, trauma involving hemorrhagic shock, and more recently, COVID-19-associated coagulopathy [5]. They can determine the patient’s hemostatic competence more precisely but other critical factors that control hemostasis in the body may be omitted. For example, the fluid dynamics of blood flow and blood interaction with the cells composing the vasculatures, i.e. endothelial cells and the underlying matrix. Additionally, the assays can determine the risk of the blood clotting through direct observation of platelet behaviors and coagulation, but bleeding risks are only indicated by the lack of or the reduced amount of activity. There is no direct observation of “bleeding” and hemostasis to assess patient’s hemostatic competence.
Developing human tissue engineered arterial constructs to simulate human in vivo thrombus formation
Published in Platelets, 2023
Jacob Ranjbar, Ying Yang, Alan G.S. Harper
The need for such models is critical for enhancing our understanding of the pathological mechanisms and treatment of both arterial and venous thrombosis. Whilst both involve unwanted blood clotting, arterial and venous thrombosis occur in parts of the circulatory system with significantly different structures –Arterial thrombosis is elicited by atherosclerotic plaque formation and rupture, whilst venous thrombosis is elicited by venous stasis within the pockets of venous valves. Thus in vitro models will need to accurately reproduce the differing vascular geometries, rheology, mechanical and cellular properties of the different sides of the blood circulation that contribute to these distinct pathologies. Although there are currently excellent in vitro models to study venous thrombosis currently being produced [19], in this review we will focus on the
Gastrointestinal bleeding in von Willebrand patients: special diagnostic and management considerations
Published in Expert Review of Hematology, 2023
Edwin Ocran, Nicholas L.J. Chornenki, Mackenzie Bowman, Michelle Sholzberg, Paula James
Von Willebrand Disease (VWD) is the most prevalent-inherited bleeding disorder. The disease is autosomally inherited and is caused by a deficiency or dysfunction of von Willebrand Factor (VWF), resulting in impaired blood clotting. The trait may occur in about 1% of the general population, with a symptomatic prevalence of 1 in 1000 [1]. VWF plays essential roles in normal hemostasis including the protection of coagulation factor VIII (FVIII) from early degradation, the binding to exposed subendothelial collagen at sites of vascular injury, and the binding to platelet surface glycoproteins, which leads to platelet adhesion and subsequent platelet aggregation under high shear stress [2,3]. Recently, VWF has been linked to other non-hemostatic roles including inflammation, cell proliferation and angiogenesis, as discussed by Rauch et al. [3].