thromboplastin and Shock

Disseminated intravascular coagulation (DIC) of blood develops as a result of a sharp increase in the release of thromboplastic substances. The mechanism of disseminated thrombosis is switched in at the level of the microcirculatory bed with defibrination of the peripheral blood and subsequent hemorrhages and bleedings. The causes of DIC development may include complications of pregnancy and delivery, different kinds of shock including endotoxin shock, hemorrhage, hemolysis. Histomorphological findings in DIC are as follows: hemorrhagic syndrome, fibrin thrombi in capillaries, arterioles and venules of the skin, kidneys, adrenals, hypophysis, gastrointestinal tract, lungs and other organs followed by necroses and hemorrhages in these organs. Clinically, DIC is manifested by symptoms of insufficiency of the affected organs (acute renal insufficiency, Waterhouse-Fridericksen syndrome, etc).

Topics: Disseminated Intravascular Coagulation; Female; Hemolysis; Hemorrhage; Humans; Kidney; Male; Microcirculation; Necrosis; Obstetric Labor Complications; Pregnancy; Pregnancy Complications, Hematologic; Shock; Surgical Procedures, Operative; Thromboplastin; Thrombosis

Topics: Animals; Antifibrinolytic Agents; Blood Coagulation; Blood Coagulation Factors; Diagnosis, Differential; Disseminated Intravascular Coagulation; Dogs; Fibrinolysis; Heparin; Humans; Liver; Platelet Adhesiveness; Shock; Thrombin; Thromboplastin; Thrombosis

Topics: Adult; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Blood Flow Velocity; Child; Child, Preschool; Clinical Laboratory Techniques; Dextrans; Female; Fibrinolytic Agents; Glomerulonephritis; Hemangioma, Cavernous; Heparin; Humans; Infections; Liver Cirrhosis; Male; Mycoses; Parasitic Diseases; Pregnancy; Pregnancy Complications; Purpura; Shock; Thrombocytopenia; Thromboplastin; Uremia

It has been observed that trauma patients often display elevated procoagulant activity that could be caused, in part, by tissue factor (TF). We previously observed that trauma patients with thermal, blunt, and penetrating injuries have active FIXa and FXIa in their plasma. In the current study, we evaluated the effect of injury severity, with or without accompanying shock, on the frequency and concentration of TF, FIXa, and FXIa in plasma from trauma patients.. Eighty trauma patients were enrolled and divided equally into four groups based on their Injury Severity Score and base deficit:Blood was collected at a 0 time-point (first blood draw upon arrival at hospital) and citrate plasma was prepared, frozen, and stored at -80 °C. FXIa, FIXa, and TF activity assays were based on a response of thrombin generation to corresponding monoclonal inhibitory antibodies.. The frequency and median concentrations of TF were relatively low in non-severe injury groups (17.5% and 0 pM, respectively) but were higher in those with severe injury (65% and 0.5 pM, respectively). Although FXIa was observed in 91% of samples and was high across all four groups, median concentrations were highest (by approximately fourfold) in groups with shock. FIXa was observed in 80% of plasma samples and concentrations varied in a relatively narrow range between all four groups. No endogenous activity was observed in plasma from healthy individuals.. (1) Frequency and concentration of TF is higher in patients with a higher trauma severity. (2) Concentration of FXIa is higher in patients with shock. (3) For the first time reported, the vast majority of plasma samples from trauma patients contain active FIXa and FXIa.. Prognostic/epidemiological study, level II.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Case-Control Studies; Factor IXa; Factor XIa; Female; Humans; Injury Severity Score; Male; Middle Aged; Shock; Thromboplastin; Wounds and Injuries; Young Adult

To obtain better insight into the pathogenesis of verotoxin-producing Escherichia coli-associated diseases, in this study, we explored the effect of verotoxin 2 (VT2) on coagulation in an animal model. After being given VT2 (50 ng/kg, lethal dose), C57BL/6 mice showed progressively increasing expression of TF mRNA in the kidney and brain and elevated plasma levels of thrombin-antithrombin III complex (TAT), normotest, fibrinogen, and PAI-1 paralleling the disease course over 24 hours; platelet counts were decreased at 48 hours with hemorrhage in the kidney and brain. Co-administration of lipopolysaccharide (LPS, 0.5 mg/kg) with VT2 (50 ng/kg) exhibited more prominant and/or prolonged increase in not only expression of TF and PAI-1 mRNAs in the kidney and brain but also plasma levels of TAT, fibrinogen, and PAI-1 and was associated with more remarkable hemorrhage in the tissues. Although VT2 (5 ng/kg) was not a lethal dose, co-administration of LPS (0.5 mg/kg) with VT2 (5 ng/kg) enhanced the susceptibility to VT2, resulting in more prolonged elevation of TAT levels during the first 24 hours than that in the LPS group and a second elevation at 72 hours, followed by death. Plasma IL-1beta level reached a maximum at 24 hours after VT2 (50 ng/kg) injection prior to the increase in TAT levels, whereas the increase in TNFalpha level immediately after injection was associated with the increase in PAI-1 mRNA. These observations indicate that the activation of coagulation by VT2 may occur through a mechanism different from that used by LPS, since plasma TAT levels rose in the mice immediately after LPS injection and returned to normal over 36 hours.

Topics: Animals; Antithrombin III; Blood Coagulation; Blood Coagulation Tests; Brain; Cytokines; Dose-Response Relationship, Drug; Drug Therapy, Combination; Fibrinogen; Hemorrhage; Intracranial Hemorrhages; Kidney; Lipopolysaccharides; Male; Mice; Mice, Inbred C57BL; Models, Animal; Neutrophils; Peptide Hydrolases; Plasminogen Activator Inhibitor 1; Platelet Count; RNA, Messenger; Shiga Toxin 2; Shock; Thromboplastin; Time Factors; Tissue Distribution

Topics: Animals; Blood Coagulation; Cat Diseases; Cats; Disseminated Intravascular Coagulation; Diuresis; Dog Diseases; Dogs; Fibrin Fibrinogen Degradation Products; Fibrinolysis; Heparin; Ischemia; Kidney; Platelet Aggregation; Shock; Thromboplastin; Urine

Topics: Acid-Base Equilibrium; Blood; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Tests; Buffers; Disseminated Intravascular Coagulation; Factor V; Factor VII; Humans; Hydrogen-Ion Concentration; Prothrombin; Shock; Thrombelastography; Thrombin; Thromboplastin

Topics: Animals; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Platelets; Disseminated Intravascular Coagulation; Embolism; Female; Humans; Leukemia; Male; Postoperative Complications; Pregnancy; Pregnancy Complications, Hematologic; Shock; Thromboplastin; Thrombosis; Wounds and Injuries

Topics: Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Humans; Oxygen Consumption; Prothrombin Time; Pulmonary Edema; Sepsis; Shock; Thromboplastin

Topics: Acute Kidney Injury; Anti-Bacterial Agents; Blood Coagulation Disorders; Endotoxins; Histamine Release; Humans; Hypotension; Hypoxia; Intestinal Absorption; Ischemia; Mononuclear Phagocyte System; Pulmonary Atelectasis; Shock; Shock, Septic; Thromboplastin

Topics: Abruptio Placentae; Afibrinogenemia; Blood Coagulation Disorders; Embolism, Amniotic Fluid; Female; Humans; Obstetric Labor Complications; Postpartum Hemorrhage; Pregnancy; Pregnancy Complications; Shock; Thromboplastin; Tissue Extracts

Topics: Animals; Blood Coagulation; Blood Platelets; Catecholamines; Humans; Hypoxia; Microscopy, Electron; Shock; Shock, Septic; Thromboembolism; Thromboplastin; Wounds and Injuries

Topics: Anticoagulants; Blood Coagulation Disorders; Blood Coagulation Tests; Coronary Vessels; Factor VIII; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Prednisone; Shock; Spondylitis, Ankylosing; Thromboplastin

Topics: Animals; Blood Coagulation Disorders; Burns; Heparin; Infusions, Parenteral; Injections; Injections, Intravenous; Mice; Prothrombin Time; Research; Shock; Skin; Thromboplastin; Tissue Extracts

Topics: Afibrinogenemia; Ammonium Compounds; Animals; Anti-Infective Agents, Local; Blood Coagulation Disorders; Deoxyribonuclease I; Disseminated Intravascular Coagulation; Dogs; Fibrinolysis; Liver Circulation; Pathology; Pulmonary Circulation; Quaternary Ammonium Compounds; Research; Shock; Shock, Hemorrhagic; Streptodornase and Streptokinase; Streptokinase; Thrombin; Thromboplastin

Topics: Animals; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Platelets; Dogs; Fibrinogen; Fibrinolysin; Hemolysis; Heparin; Prothrombin Time; Research; Shock; Shock, Hemorrhagic; Silicones; Thromboplastin