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Endothelial Cells and Hemodynamics
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Elazer Edelman, Farhad Rikhtegar Nezami
Endothelial cell dysfunction triggered by different stimuli perturbs the hemostasis-mediating balance between procoagulant and anticoagulant factors. Inflammation and endothelial cell dysfunction are directly related to all stages of atherosclerosis, thrombosis and related complications (Bergan et al., 2006; Chiu et al., 2009; Dimmeler et al., 2002; Garin and Berk, 2006; Gimbrone, 1995; Ross and Glomset, 1976; Topper and Gimbrone Jr., 1999). The permeability and thus the function of damaged/dysfunctional endothelium is significantly altered as the dysfunctional endothelial cell layer is activated by cardiovascular risk factors (Libby et al., 2010). Intercellular junctions (identified primarily as tight, gap and adherence junctions), the most important regulators of endothelium integrity and permeability, are modulated by several biological factors including inflammatory mediators (Bordron et al., 1998; Khazaei and Nematbakhsh, 2004). Consequently, transportation of macromolecules through endothelial junctions is significantly altered in response to inflammatory mediators, increasing their permeability (Lum and Malik, 1994, 1996). Increased permeability opens the gateway to lipoproteins, monocytes and macrophages, triggering smooth muscle cell migration and proliferation (Celermajer, 1997) and promoting an atherosclerotic plaque initiation and progression (Davignon and Ganz, 2004; Ross, 1999).
Von Willebrand Disease
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
As a patient progresses through pregnancy, many of the values used for diagnosis are normal due to the procoagulant state of pregnancy, thus diagnosis cannot be made reliably. For distinguishing types (Table 16.1) also send multimeric analysis and factor VIII binding assay. Factor VIII levels are best (but not that good) at predicting surgical/soft-tissue bleeding.
Shock Management
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
Fibrinogen is the key procoagulant factor needed for stable clot formation and the earliest clotting protein to fall during active major bleeding. The ongoing CRYOSTAT-2 randomized controlled trial95 is evaluating whether early administration of high-dose cryoprecipitate, in addition to standard major haemorrhage therapy, improves survival from traumatic bleeding. The results from this trial may well inform future transfusion resuscitation practice.
Asprosin is positively associated with metabolic syndrome in hemodialysis patients: a cross-sectional study
Published in Renal Failure, 2023
Jiandong Zhou, Weijie Yuan, Yunshan Guo, Yongfang Wang, Yuyang Dai, Ying Shen, Xuan Liu
Fasting blood samples were collected before starting dialysis after one day without a dialysis session. Blood was added to tubes containing procoagulant to obtain serum. Samples were processed within 2 h of collection and centrifuged at 3000 × g for 5 min. Serum albumin, transaminase, urea nitrogen, creatinine, lipids, calcium, phosphate and iPTH levels were determined by routine laboratory methods. Aliquots of serum were prepared and immediately stored at −20 °C until assay. Serum asprosin levels were determined using a commercially available enzyme-linked immunosorbent assay (Cat: AE59067HU, Abebio, Wuhan, China). Samples were diluted 500-fold, following the manufacturer’s recommendations. All samples were analyzed in duplicate and the average of these values was used for calculations.
Diabetes type 2: relationships between lysosomal exocytosis of circulating normal-sized platelets and in vitro ɑ-thrombin-evoked platelet responses
Published in Annals of Medicine, 2023
Maria Edvardsson, Magnus Oweling, Petter Järemo
Community-dwelling seniors who visited an outpatient clinic for type 2 diabetes were enrolled. We wanted to study a procoagulant condition with respect to differences within the diseased group so we did not include healthy individuals as controls; therefore, our findings could be features of disease or they may occur in health as well. The participants were heterogeneous with respect to comorbidities and medications (Table 1), which may have influenced the results. As judged from the medications (Table 1), elevated cholesterol and hypertension were common. When providing consent, some patients were taking either ADP receptor blockers (n = 1) or aspirin (n = 6). Platelet ɑ-thrombin responses were unrelated to aspirin (data not shown), but clopidogrel affects agonist-evoked platelet WB activity [28].
Application of anti-Xa assay in monitoring unfractionated heparin therapy in contemporary antithrombotic management
Published in Expert Review of Hematology, 2023
Michael Safani, Steve Appleby, Ryan Chiu, Emmanuel J Favaloro, Emanuel T. Ferro, Jimmy Johannes, Milan Sheth
The coagulation pathways represent a cascade of events intended to provide a balance between procoagulant and anticoagulant processes and maintain hemostasis. Primary hemostasis consists of platelet activation, aggregation, and thrombus formation and aims to form a plug at the site of exposed endothelial cells due to tissue damage. Secondary hemostasis, as measured by the pathology laboratory, conventionally comprises three coagulation pathways. The intrinsic pathway is activated by endothelial damage and collagen exposure and includes factors I, II, IX, X, XI, and XII. The extrinsic pathway is activated by release of tissue factor by damaged endothelium and includes factors I, II, VII, and X. The common pathway consists of factors I, II, V, VIII, X. The intrinsic and extrinsic pathways converge to form a common pathway and at a specific point to activate fibrinogen to form fibrin polymer. In vivo, the final stages of primary and secondary hemostasis are marked by binding of fibrin polymers to platelets to secure and stabilize the platelet plug [37–41].