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Hemostatic Function (hemostatic + function)
Selected AbstractsOral melatonin reduces blood coagulation activity: a placebo-controlled study in healthy young menJOURNAL OF PINEAL RESEARCH, Issue 2 2008Petra H. Wirtz Abstract:, Melatonin has previously been suggested to affect hemostatic function but studies on the issue are scant. We hypothesized that, in humans, oral administration of melatonin is associated with decreased plasma levels of procoagulant hemostatic measures compared with placebo medication and that plasma melatonin concentration shows an inverse association with procoagulant measures. Forty-six healthy men (mean age 25 ± 4 yr) were randomized, single-blinded, to either 3 mg of oral melatonin (n = 25) or placebo medication (n = 21). One hour thereafter, levels of melatonin, fibrinogen, and D-dimer as well as activities of coagulation factor VII (FVII:C) and VIII (FVIII:C) were measured in plasma. Multivariate analysis of covariance and regression analysis controlled for age, body mass index, mean arterial blood pressure, heart rate, and norepinephrine plasma level. Subjects on melatonin had significantly lower mean levels of FVIII:C (81%, 95% CI 71,92 versus 103%, 95% CI 90,119; P = 0.018) and of fibrinogen (1.92 g/L, 95% CI 1.76,2.08 versus 2.26 g/L, 95% CI 2.09,2.43; P = 0.007) than those on placebo explaining 14 and 17% of the respective variance. In all subjects, increased plasma melatonin concentration independently predicted lower levels of FVIII:C (P = 0.037) and fibrinogen (P = 0.022) explaining 9 and 11% of the respective variance. Melatonin medication and plasma concentration were not significantly associated with FVII:C and D-dimer levels. A single dose of oral melatonin was associated with lower plasma levels of procoagulant factors 60 min later. There might be a dose,response relationship between the plasma concentration of melatonin and coagulation activity. [source] Platelet function in sepsisJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 12 2004A. YAGUCHI Summary.,Background: Coagulation abnormalities and thrombocytopenia are common in severe sepsis, but sepsis-related alterations in platelet function are ill-defined. Objectives: The purpose of this study was to elucidate the effect of sepsis on platelet aggregation, adhesiveness, and growth factor release. Patients and methods: Agonist-induced platelet aggregation was measured in platelet-rich plasma separated from blood samples collected from 47 critically ill patients with sepsis of recent onset. Expression of platelet adhesion molecules was measured by flow cytometry and the release of vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) was measured by ELISA in the supernatant of platelet aggregation. Results: Septic patients had consistently decreased platelet aggregation compared with controls, regardless of the platelet count, thrombin generation, or overt disseminated intravascular coagulation (DIC) status. The severity of sepsis correlated to the platelet aggregation defect. Adhesion molecules, receptor expression (CD42a, CD42b, CD36, CD29, PAR-1), and ,-granule secretion detected by P-selectin expression remained unchanged but the release of growth factors was differentially regulated with increased VEGF and unchanged PDGF after agonist activation even in uncomplicated sepsis. Conclusions: Sepsis decreases circulating platelets' hemostatic function, maintains adhesion molecule expression and secretion capability, and modulates growth factor production. These results suggest that sepsis alters the hemostatic function of the platelets and increases VEGF release in a thrombin-independent manner. [source] Dementia in subjects with atrial fibrillation: hemostatic function and the role of anticoagulationJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 11 2004M. Barber Summary.,Background: Atrial fibrillation (AF) is associated with cognitive impairment and dementia, perhaps through encouraging a prothrombotic state and cardioembolism. Objectives: We wished to test the hypotheses that hemostatic function is altered in subjects with AF who develop dementia, and that long-term warfarin anticoagulation is protective against this complication. Patients and methods: Recruitment was from an observational cohort study of AF. Baseline assessment included measurement of plasma fibrinogen, fibrin D -dimer, prothrombin fragment 1+2 (F1+2), thrombin,antithrombin complexes (TAT), von Willebrand factor and tissue plasminogen activator. We assessed cognitive function after 3 years' follow-up using the 13-item modified Telephone Interview for Cognitive Status (TICSm) and the short form of the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Results: Of the 218 subjects assessed, 145 (66%) were prescribed warfarin. Forty-nine (22%) met TICSm/IQCODE criteria for dementia. D -dimer, F1+2 and TAT levels were higher in AF subjects with dementia compared with those without (medians 81 vs. 60 ng mL,1, P = 0.008; 0.76 vs. 0.49 nmol L,1, P = 0.006; and 1.78 vs. 1.44 µg L,1, P = 0.003, respectively). These associations became of borderline statistical significance following adjustment for age. Logistic regression showed a trend towards warfarin use being independently associated with reduced prevalence of dementia (odds ratio 0.52, P = 0.08). Conclusions: We found evidence of increased thrombin generation and fibrin turnover in subjects with AF and dementia compared with those without dementia. Long-term warfarin use may be protective against the development of dementia in subjects with AF. [source] Hemostatic and hematological abnormalities in gain-of-function fps/fes transgenic mice are associated with the angiogenic phenotypeJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 11 2004W. Sangrar Summary. The Fps/Fes tyrosine kinase has been implicated in the regulation of hematopoiesis and inflammation. Mice expressing an activated variant of Fps/Fes (MFps) encoded by a gain-of-function mutant transgenic fps/fes allele (fpsMF) exhibited hematological phenotypes, which suggested that Fps/Fes can direct hematopoietic lineage output. These mice also displayed marked hypervascularity and multifocal-hemangiomas which implicated this kinase in the regulation of angiogenesis. Here we explored the potential involvement of Fps/Fes in the regulation of hemostasis through effects on blood cells and the vascular endothelium. Hematological parameters of fpsMF mice were characterized by peripheral blood analysis, histology, and transmission electron microscopy. Hemostasis parameters and platelet functions were assessed by flow cytometry and measurements of activated partial thromboplastin time, prothrombin time, thrombin clot time, platelet aggregation, bleeding times and in vitro fibrinolytic assays. Hematological and morphological analyses showed that fpsMF mice displayed mild thrombocytopenia, anemia, red cell abnormalities and numerous hemostatic defects, including hypofibrinogenemia, hyper-fibrinolysis, impaired whole blood aggregation and a mild bleeding diathesis. fpsMF mice displayed a complex array of hemostatic perturbations which are reminiscent of hemostatic disorders such as disseminated intravascular coagulation (DIC) and of hemangioma-associated pathologies such as Kasabach,Merritt phenomenon (KMS). These studies suggest that Fps/Fes influences both angiogenic and hemostatic function through regulatory effects on the endothelium. [source] Perioperative Monitoring of Thromboelastograph on Hemostasis and Therapy for Cyanotic Infants Undergoing Complex Cardiac SurgeryARTIFICIAL ORGANS, Issue 11 2009Yongli Cui Abstract This study investigated features and treatments of perioperative coagulopathies in cyanotic infants with complex congenital heart disease (CCHD). Thirty-six infants with cyanotic CCHD were involved and divided into two groups: In group H (n = 20), hematocrit (HCT) > 54%, and in group L (n = 16), HCT < 54%. Blood was sampled at anesthesia induction (T1), rewarming to 36°C (T2), after heparin neutralization (T3), and 4 h after operation (T4). The hemostatic changes were evaluated by thromboelastograph (TEG). After surgery, group H was treated with fibrinogen-combined platelets (PLT), while group L was treated with PLT only. We observed the effect at T4. At T1, the hemostatic function in group H, deteriorating with the increase of HCT (P < 0.01), was obviously lower than that in group L (P < 0.01), but the PLT function was still complete. In group H, the hemostatic function at T2 decreased with a significant drop of PLT function (P < 0.01) and had little change of functional fibrinogen (Ffg) (P > 0.05). At T3, compared with T2, there were improvements in hemostatic function and Ffg (P < 0.01, respectively) without increase of PLT (P > 0.05) in group H. After therapy, PLT function in both groups restored to T1 level (P > 0.05); Ffg at T4 was significantly better than at T1 (P < 0.01) in group H, but Ffg at T4 with still normal function was lower than at T1 in group L (P < 0.01). Whole hemostatic function at T4 was back to normal and had no differences between two groups. So, we proposed that fibrinogen and PLT transfusion in combination should be better for infants with high HCT CCHD, but PLT alone might be enough for low HCT ones. 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