fibrin and Acidosis

fibrin has been researched along with Acidosis* in 5 studies

Other Studies

5 other study(ies) available for fibrin and Acidosis

ArticleYear
Effects of an acidic environment on coagulation dynamics.
    Journal of thrombosis and haemostasis : JTH, 2016, Volume: 14, Issue:10

    Essentials Acidosis, an outcome of traumatic injury, has been linked to impaired procoagulant efficiency. In vitro model systems were used to assess coagulation dynamics at pH 7.4 and 7.0. Clot formation dynamics are slightly enhanced at pH 7.0 in blood ex vivo. Acidosis induced decreases in antithrombin efficacy offset impairments in procoagulant activity.. Background Disruption of hydrogen ion homeostasis is a consequence of traumatic injury often associated with clinical coagulopathy. Mechanisms by which acidification of the blood leads to aberrant coagulation require further elucidation. Objective To examine the effects of acidified conditions on coagulation dynamics using in vitro models of increasing complexity. Methods Coagulation dynamics were assessed at pH 7.4 and 7.0 as follows: (i) tissue factor (TF)-initiated coagulation proteome mixtures (±factor [F]XI, ±fibrinogen/FXIII), with reaction progress monitored as thrombin generation or fibrin formation; (ii) enzyme/inhibitor reactions; and (iii) TF-dependent or independent clot dynamics in contact pathway-inhibited blood via viscoelastometry. Results Rate constants for antithrombin inhibition of FXa and thrombin were reduced by ~ 25-30% at pH 7.0. At pH 7.0 (+FXI), TF-initiated thrombin generation showed a 20% increase in maximum thrombin levels and diminished thrombin clearance rates. Viscoelastic analyses showed a 25% increase in clot time and a 25% reduction in maximum clot firmness (MCF). A similar MCF reduction was observed at pH 7.0 when fibrinogen/FXIII were reacted with thrombin. In contrast, in contact pathway-inhibited blood (n = 6) at pH 7.0, MCF values were elevated 6% (95% confidence interval [CI]: 1%-11%) in TF-initiated blood and 15% (95% CI: 1%- 29%) in the absence of TF. Clot times at pH 7.0 decreased 32% (95% CI: 15%-49%) in TF-initiated blood and 51% (95% CI: 35%-68%) in the absence of TF. Conclusions Despite reported decreased procoagulant catalysis at pH 7.0, clot formation dynamics are slightly enhanced in blood ex vivo and suppression of thrombin generation is not observed. A decrease in antithrombin reactivity is one potential mechanism contributing to these outcomes.

    Topics: Acidosis; Antithrombin III; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Tests; Elasticity; Fibrin; Fibrinogen; Healthy Volunteers; Humans; Hydrogen-Ion Concentration; Ions; Proteome; Thrombin; Thromboplastin; Time Factors; Viscosity

2016
Potential of whole blood coagulation reconstitution by desmopressin and fibrinogen under conditions of hypothermia and acidosis--an in vitro study using rotation thrombelastometry.
    Scandinavian journal of clinical and laboratory investigation, 2011, Volume: 71, Issue:4

    Desmopressin (DDAVP) and fibrinogen improve platelet function and clot stability. We investigated the influence of DDAVP and fibrinogen on whole blood coagulation in an in vitro model of hypothermia and acidosis.. After IRB approval and written consent blood samples were taken from 10 healthy volunteers. Samples were prepared with hydrochloric acid to maintain--beside normal pH--reduced pH (∼7.2) and severely reduced pH (∼7.0), and were assigned to four treatment groups: addition of either isotonic saline for compensation of dilutional effects (ISO), desmopressin (DDAVP+), fibrinogen (FIB+), or both substances (DDAVP+FIB+). Baseline was ISO at 37°C and normal pH. Remaining samples were incubated for 30 min and measured at 32°. Rotation thrombelastometry (ROTEM) after extrinsically activation and fibrin polymerization was tested. Repeated measures ANOVA were performed (p < 0.05).. Hypothermia and acidosis synergistically impaired whole blood coagulation. DDAVP+ normalized maximum clot firmness (MCF) at normal pH. Coagulation time (CT) was not affected. FIB+ normalized MCF at pH 7.35 and pH 7.2. CT was normalized independently of pH. DDAVP+FIB+ did not show additional effects to FIB+. Fibrin polymerization was increased by FIB+ and DDAVP+FIB+ independently of pH. DDAVP+ did not alter fibrin polymerization.. DDAVP and fibrinogen increased whole blood coagulation under hypothermia. Acidosis diminished this effect. Thus, acidosis should be corrected first and then both substances could be used for bridging until normothermia can be achieved. In combination, the effects of fibrinogen were overwhelming DDAVP effects. Thus, combined administration did not show any benefit compared to fibrinogen administration alone.

    Topics: Acidosis; Adult; Blood Coagulation; Deamino Arginine Vasopressin; Female; Fibrin; Fibrinogen; Humans; Hypothermia; Male; Protein Multimerization; Thrombelastography; Whole Blood Coagulation Time

2011
Hypothermia and acidosis synergistically impair coagulation in human whole blood.
    Anesthesia and analgesia, 2008, Volume: 106, Issue:6

    Hypothermia and acidosis were reported to influence coagulopathy in different clinical settings. We evaluated whole blood coagulation to determine the effects of hypothermia and/or acidosis on hemostasis.. Whole blood samples (3.000 microL) from 10 healthy volunteers (2 female, 8 male) were acidified by adding 40 microL of hydrochloric acid of increasing molarity to achieve a blood pH (alpha-stat) between 7.0 and 7.37, and coagulation was analyzed by rotational thromboelastometry after an incubation period of 30 min using both intrinsically (InTEM) and extrinsically (ExTEM) activated assays. To assess temperature-dependent effects, all tests were performed at blood/thromboelastometer temperatures of 30, 33, 36, and 39 degrees C, respectively. An additional extrinsically activated test with addition of cytochalasin D was performed to examine clot formation without platelet contribution.. Hypothermia at a normal pH produced an increased coagulation time [ExTEM: 65 s +/- 3.6 (36 degrees C) vs 85 +/- 4 (30 degrees C), P < 0.001; coagulation time, InTEM: 181 s +/- 10 (36 degrees C) vs 226 +/- 9, P < 0.001] and clot formation time [ExTEM: 105 s +/- 5 (36 degrees C) vs 187 +/- 6 (30 degrees C), P < 0.001]; clot formation time [InTEM: 101 s +/- 5 (36 degrees C) vs 175 +/- 7, P < 0.001], as well as decreased alpha angle [ExTEM: 65.6 +/- 1.8 (36 degrees C) vs 58 +/- 1.1, P < 0.01, P < 0.01; InTEM: 70.5 +/- 1.8 (36 degrees C) vs 60.2 +/- 1.5, P < 0.001]. Maximum clot firmness was significantly impaired only in InTEM assays [56.9 mm +/- 0.9 (36 degrees C) vs 52.7 +/- 0.9, P < 0.05]. In contrast, acidosis per se had no significant effects during normothermia. Acidosis amplified the effects of hypothermia, and synergistically impaired clotting times, alpha angle, and decreased maximum clot firmness, again in both extrinsically and intrinsically activated assays. Formation of a fibrin clot tested after abolition of platelet function by cytochalasin D was not impaired. Clot lysis decreased under hypothermic and/or acidotic conditions, but increased with hyperthermia.. In this in vitro study, hypothermia produced coagulation changes that were worsened by acidosis whereas acidosis without hypothermia has no significant effect on coagulation, as studied by thromboelastometry. This effect was mediated by the inhibition of coagulation factors and platelet function. Thus, thromboelastometry performed at 37 degrees C overestimated integrity of coagulation during hypothermia in particular in combination with acidosis.

    Topics: Acidosis; Adult; Blood Coagulation; Blood Coagulation Tests; Blood Platelets; Cytochalasin D; Female; Fibrin; Humans; Hydrogen-Ion Concentration; Hypothermia; Male; Reproducibility of Results; Temperature

2008
Effects of acidosis on fetal and maternal blood coagulation: a fetal lamb model.
    Pediatric research, 1985, Volume: 19, Issue:1

    The effects of fetal acidosis (mean pH 6.93) on fetal and maternal blood coagulation were measured. Test results from 10 fetal lambs and mother ewes (127 +/- 2 days mean gestation) before and after fetal lactic acid infusions were compared to test results from eight control fetal lambs and mother ewes (127 +/- 3 days mean gestation) before and after control glucose infusion. Significant changes found in acidotic fetal lambs not seen in control fetuses included an increase in the white blood cell count (mean 2800/mm3 before to 3600/mm3 after acidosis; p = 0.0009), a shortening of the thrombin time (mean 17.8 s before to 11.2 s after acidosis; p = 0.0001), and decreases in the activities of factor V (mean 57% before to 37% after acidosis; p = 0.0014) and factor IX (mean 35% before to 29% after acidosis; p = 0.0128). There was also a reduction in the concentration of fibrinogen (mean 147 mg/100 ml before to 125 mg/100 ml after acidosis; p = 0.0492) but no significant changes in the levels of fibrin monomer, fibrinogen/fibrin degradation products, or antithrombin III. In vitro exposure of five different fetal whole blood samples to a pH of 6.9 for 2 h at 37 degrees C did not result in significant changes in any of the coagulation factor activities. A significant decrease in the level of factor V was also found in the mother ewes of the acidotic fetuses (mean 141% before to 113% after acidosis; p = 0.006) and a decrease in the level of maternal factor IX approached significance (mean 119% before to 102% after acidosis; p = 0.0564).(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Acidosis; Animals; Animals, Newborn; Antithrombin III; Blood Coagulation Factors; Blood Coagulation Tests; Female; Fibrin; Fibrinogen; Gestational Age; Lactates; Lactic Acid; Maternal-Fetal Exchange; Platelet Count; Pregnancy; Sheep

1985
Hyperalimentation in cirrhotic patients.
    American journal of surgery, 1972, Volume: 123, Issue:1

    Topics: Acid-Base Equilibrium; Acidosis; Alanine Transaminase; Alkaline Phosphatase; Amino Acids; Ammonia; Arginine; Carbon Dioxide; Caseins; Catheterization; Cysteine; Diet Therapy; Fibrin; Glutamine; Glycine; Histidine; Humans; Isoleucine; Leucine; Liver; Liver Cirrhosis; Lysine; Methionine; Parenteral Nutrition; Phenylalanine; Potassium; Sodium; Threonine; Tryptophan

1972
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