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PubMed2005

Effects of bovine polymerized hemoglobin on coagulation in controlled hemorrhagic shock in swine.

HBOC-201, a bovine polymerized hemoglobin, has been proposed as a novel oxygen-carrying resuscitative fluid for patients with hemorrhagic shock (HS). Herein, we evaluated the hemostatic effects of HBOC-201 in an animal model of HS. A 40% blood loss-controlled hemorrhage and soft tissue injury were performed in 24 invasively monitored Yucatan mini-pigs. Pigs were resuscitated with HBOC-201 (HBOC) or hydroxyethyl starch (HEX), or were not resuscitated (NON) based on cardiac parameters during a 4-h prehospital phase. Afterward, animals received simulated hospital care for 3 days with blood or saline transfusions. Hemostasis measurements included in vivo bleeding time (BT), thromboelastography (TEG), in vitro bleeding time (platelet function; PFA-CT), prothrombin time (PT), and partial thromboplastin time (PTT). Serum lactate was measured and lung sections were evaluated for microthrombi by electron microscopy. During the prehospital phase, BT remained unchanged in the HBOC group. TEG reaction time increased in HBOC pigs during the late prehospital phase and was greater than in NON or HEX pigs at 24 h (P = 0.03). TEG maximum amplitude was similar for the two fluid-resuscitated groups. PFA-CT increased in both resuscitated groups but less with HBOC (P = 0.02) in the prehospital phase; this effect was reversed by 24 h (P = 0.02). In the hospital phase, PT decreased (P < 0.02), whereas PTT increased above baseline (P < 0.01). Lactic acidosis in HBOC and HEX groups was similar. Aspartate aminotransferase was relatively elevated in the HBOC group at 24 h. Electron microscopy showed no evidence of platelet/fibrin clots or microthrombi in any of the animals. Twenty-four-hour group differences mainly reflected the fact that all HEX animals (8/8) received blood transfusions compared with only one HBOC animal (1/8). In swine with HS, HBOC resuscitation induced less thrombopathy than HEX during the prehospital phase. Mild delayed effects on platelet and clot formation during the hospital phase are transient and likely related to fewer blood transfusions. In swine with HS, HBOC resuscitation induced less thrombopathy than HEX during the prehospital phase but more thrombopathy in the hospital phase. The delayed effects on platelet and clot formation during the hospital phase are transient and may be related to the need for fewer blood transfusions.

Acidosis, Lactic↗
PubMed2004

In vitro effects of poly-N-acetyl glucosamine on the activation of platelets in platelet-rich plasma with and without red blood cells.

BACKGROUND: This study was performed to assess the effect of poly-N-acetyl glucosamine fiber slurry on plasma clotting proteins, platelets, and red blood cells in the clotting of the blood. METHODS: Citrate phosphate dextrose whole blood was stored at 22degreesC for 48 hours to prepare platelet-poor plasma, platelet-rich plasma (PRP), and PRP plus red blood cells with hematocrit values of 20%, 35%, and 45% with and without an equal volume of poly-N-acetyl glucosamine fibers (1 mg/mL 0.9% NaCl). RESULTS: Thromboelastogram data show that poly-N-acetyl glucosamine fibers (p-GlcNAc) significantly reduced the R time in platelet-poor plasma, PRP, and PRP supplemented with red blood cells. Poly-N-acetyl glucosamine fibers increased, but not significantly, Annexin V and factor X binding to platelets, platelet microparticles, and red blood cell Annexin V binding. Poly-N-acetyl glucosamine fibers increased the production of thromboxane B2 by PRP. CONCLUSION: Poly-N-acetyl glucosamine slurry activates platelets.

Acetylglucosamine↗
PubMed2005

Hypercoagulability is most prevalent early after injury and in female patients.

BACKGROUND: Hypercoagulability after injury is a major source of morbidity and mortality. Recent studies indicate that there is a gender-specific risk in trauma patients. This study was performed to determine the course of coagulation after injury and to determine whether there is a gender difference. We hypothesized that hypercoagulability would occur early after injury and that there would be no difference between men and women. METHODS: This was a prospective cohort study. Inclusion criteria were admission to the intensive care unit, Injury Severity Score > 4, and the ability to obtain consent from the patient or a relative. A Thrombelastograph (TEG) analysis was performed and routine coagulation parameters and thrombin-antithrombin complexes were measured within 24 hours of injury and then daily for 4 days. RESULTS: Sixty-five patients met criteria for entry into the study. Their mean age was 42 +/- 17 years and their mean Injury Severity Score was 23 +/- 12. Forty patients (62%) were men. The prevalence of a hypercoagulable state by TEG was 62% on day 1 and 26% on day 4 (p < 0.01). Women were significantly more hypercoagulable on day 1 than men as measured by the time to onset of clotting (women, 2.9 +/- 0.7 minutes; men, 3.9 +/- 1.5 minutes; p < 0.01; normal, 3.7-8.3 minutes). Mean platelet counts, international normalized ratios, and partial thromboplastin times were within normal limits throughout the study. Thrombin activation as measured by thrombin-antithrombin complexes decreased from 34 +/- 15 microg/L on day 1 to 18 +/- 8 microg/L (p < 0.01) on day 4, consistent with the prevalence of hypercoagulability by TEG. CONCLUSION: Hypercoagulability after injury is most prevalent during the first 24 hours. Women are more hypercoagulable than men early after injury. The TEG is more sensitive than routine coagulation assays for the detection of a hypercoagulable state.

Adult↗
PubMed2006

Acidosis impairs the coagulation: A thromboelastographic study.

BACKGROUND: Coagulopathy is a contributor to and predictor of death in bleeding patients. Acidosis is known to be a predictor of worse outcome in trauma patients and to be a coexisting factor in coagulopathic patients, but it has not been studied if it is a causal factor in the development of coagulopathy. METHODS: We have adjusted the pH level in blood samples from healthy volunteers to different levels between 7.4 and 6.8 by the use of hydrochloric acid. Thereafter we have studied the coagulation at the different pH levels by the use of thromboelastography. RESULTS: We found a strong correlation between pH levels and impairment of the coagulation, where the clot strength is increased much slower at pH levels below 7.4 even though the initiation of the clotting seems to be normal. The clot formation time was increased by 168% at pH 6.8 as compared with pH 7.4 (p < 0.00001, r = 0.89) whereas the clotting time was left unaffected. CONCLUSIONS: Acidosis causes a strong impairment of the coagulation as measured with thromboelastography. The impairment found when lowering pH from 7.4 to 7.15 was almost identical to the impairment seen in another study by Kettner et al. when the temperature was lowered from 36 degrees C to 32 degrees C.

Acidosis↗
PubMed2003

Adverse outcome of human islet-allogeneic blood interaction.

BACKGROUND: A report of inflammatory damage when islets come into contact with allogeneic blood prompted us to confirm the finding. METHODS: Fresh handpicked human islets were incubated in blood group matched, nonsensitized allogeneic blood. Destruction was quantified by assaying the supernatants for proinsulin release and by blood clot histology. The effect on global hemostasis was assessed by thromboelastography (TEG), and heparin-bonded tubing was used to assess the effect on blood cellular counts. In separate experiments, islets were incubated in allogeneic blood with heparin or Reopro (monoclonal anti-GpIIbIIIa). Islets were also incubated in serum, and cryosections were stained for C1q, C4, C3, C5b-9, immunoglobulin (Ig)M, and IgG binding using immunohistochemistry. RESULTS: Histologic assessment showed severe destruction in 37% of islets in contact with allogeneic blood versus none in controls and a sevenfold increase in proinsulin release from controls (n = 6)(P < 0.005). TEG (n = 11) showed accelerated coagulation in the presence of islets (P < 0.001). Analysis of blood cellular counts (n = 3) showed consumption of platelets, neutrophils, and monocytes in the presence of islets (P < 0.001). Inhibition of coagulation with heparin (n = 3) or inhibition of platelet aggregation with Reopro (n = 3), separately or together (n = 3), did not make a substantial improvement in the destruction in terms of histology or proinsulin release. Immunohistochemical staining (n = 4) revealed C1q, C4, C3, and C5b-9 deposition along with IgG binding. IgM binding was weak if anything. CONCLUSION: This study confirms and extends the finding that human islet-allogeneic blood interaction results in significant destruction of islet tissue with activation of the coagulation cascade and platelet, neutrophil, and monocyte consumption. There was evidence for activation of complement by the classical pathway along with IgG binding.

Abciximab↗
PubMed2006

Ethanol impairs coagulation and fibrinolysis in whole blood: a study performed with rotational thromboelastometry.

The objective was to study the effects of ethanol on coagulation and fibrinolysis in whole blood. Blood samples from healthy volunteers were analyzed before and after in-vitro addition of ethanol in order to achieve ethanol concentrations of 0, 1, 2 and 4 per thousand, respectively (0, 22, 44 and 88 mmol/l). Coagulation and fibrinolysis were then assessed using rotational thromboelastometry. We found that increasing ethanol levels increasingly impaired coagulation as evaluated with rotational thromboelastometry, with a maximum prolongation of the clot formation time of 118% at an ethanol level of 4 per thousand (P < 0.000001). We also found a very strong impairment of fibrinolysis already at an ethanol level of 1 per thousand. This is the first study assessing the effects of ethanol on coagulation and fibrinolysis in a whole blood model. The impairment of coagulation is similar in nature to the impairment found in patients suffering from hypothermia. The impairment is at a level that may be of clinical importance (e.g. in patients suffering from trauma). The inhibition of fibrinolysis is obvious already at an ethanol level of 1 per thousand and it may be a contributing factor to the increased amount of coronary and cerebrovascular ischemic events after binge drinking.

Alcohol Drinking↗
PubMed2003

A novel therapeutic approach combining human plasma-derived Factors VIIa and X for haemophiliacs with inhibitors: evidence of a higher thrombin generation rate in vitro and more sustained haemostatic activity in vivo than obtained with Factor VIIa alone.

BACKGROUND AND OBJECTIVES: Therapy with recombinant Factor VIIa (rFVIIa) for haemophiliacs with inhibitors still has some unresolved problems, such as the requirement for frequent infusions of rFVIIa every 2-3 h to sustain haemostatic activity for an extended time-period and that the therapeutic dose of rFVIIa is not always predictable. In the present study, we searched for an effective combination of plasma-derived FVIIa with other blood coagulation factors, and demonstrated that a therapeutic approach combining plasma-derived FVIIa and Factor X (FX) was more useful for treating haemophiliacs with inhibitors than FVIIa alone. MATERIALS AND METHODS: The haemostatic effects of FVIIa and FX were evaluated in vitro and in vivo. In in vitro experiments we assessed the following: the ability to enhance the thrombin generation rate in a reconstituted blood coagulation model without Factor VIII (FVIII) or Factor IX (FIX); the ability to correct the activated partial prothrombin time (APTT) of FVIII-depleted plasma or FIX-depleted plasma; and the ability to correct the clotting time of haemophilia-like whole blood using thromboelastography (TEG). In in vivo experiments, the haemostatic activity of the combination treatment of FVIIa and FX was determined by measuring the bleeding time and TEG using a monkey haemophilia B model produced by the injection of anti-human FIX polyclonal antibodies. The degree of thrombogenicity of the combination was evaluated using the rabbit stasis model. RESULTS: The addition of FX to FVIIa dramatically enhanced the thrombin generation rate in the reconstituted blood coagulation model and corrected the prolonged APTTs of FVIII- and FIX-depleted plasmas to levels achieved by the replacement therapies. In contrast, the addition of prothrombin to FVIIa did not show such enhancing activity. Furthermore, FVIIa-induced whole blood clotting times in the FVIII- and FIX-inhibited states were also shortened by the addition of FX in a concentration-dependent manner. Finally, the co-administration of FVIIa (80 microg/kg) and FX (800 microg/kg) in a monkey haemophilia B model resulted in a more robust and persistent haemostatic effect on the secondary bleeding time and whole-blood clotting time of TEG than that of FVIIa alone. The results of rabbit stasis tests for evaluating the risk of thrombogenicity showed that the combination of FVIIa and FX was less thrombogenic than FEIBA. CONCLUSIONS: The present study demonstrated that the combination of FVIIa and FX appeared to have a higher and more sustainable haemostatic potential than FVIIa alone, and less thrombogenicity than FEIBA. A therapeutic approach combining FVIIa and FX could be a promising and novel approach to compensate for the disadvantages of rFVIIa and FEIBA for haemophiliacs with inhibitors.

Animals↗
PubMed2004

Fibrin sealant produced by the CryoSeal FS System: product chemistry, material properties and possible preparation in the autologous preoperative setting.

BACKGROUND AND OBJECTIVES: The CryoSeal FS has been introduced as an automated device for the production of fibrin sealant from small volumes of plasma. We tested this device and compared the product with commercially available fibrin sealants and with the requirements of the European Pharmacopoeia. MATERIALS AND METHODS: The CP3 program and disposables required were used to manufacture fibrin sealant. The chemistry and mechanical properties of the product were investigated. RESULTS: The cryoprecipitate generated with CryoSeal contains concentrated fibrinogen and critical clotting factors. The efficiency of the production process is poor, but the production procedure itself is simple and not time-consuming. The volume of plasma required allows application in the preoperative autologous setting. CONCLUSIONS: The CryoSeal FS is an automated device for cryoprecipitation and production of thrombin. It can be implemented easily in the clinical routine, although, owing to product specifications, the efficacy of the CryoSeal fibrin sealant requires further clinical trials.

Blood Component Removal↗
PubMed1997

In vitro evaluation of the effect of profound haemodilution with hydroxyethyl starch 6%, modified fluid gelatin 4% and dextran 40 10% on coagulation profile measured by thromboelastography.

Synthetic colloids have been implicated as a cause of coagulopathy when administered in large quantities. The effect of profound haemodilution (50%) on coagulation profile was measured in vitro by thromboelastography. Blood samples were taken from 11 ASA grade 1 patients prior to induction of anaesthesia for elective surgery. Each sample was simultaneously tested in four different preparations: undiluted blood (control sample); blood diluted with hydroxyethyl starch 6%; blood diluted with modified fluid gelatin 4%; blood diluted with dextran 40 10%. There was a significant decrease in reaction time in the preparations treated with hydroxyethyl starch 6% and modified fluid gelatin 4%, reflecting activation of initial fibrin formation. A significant increase in clot formation time was noted in the hydroxyethyl starch 6%-treated preparations. There was also a significant decrease in clot formation rate and maximum amplitude in the hydroxyethyl starch 6% group. Clot formation time, clot formation rate and maximum amplitude did not change in the modified fluid gelatin 4% group. Profound haemodilution with dextran 40 10% exerted extreme effects on the measured variables, very often resulting in a straight line on the thromboelastography profile.

Blood Coagulation↗
PubMed2005

Effect of amniotic fluid on coagulation and platelet function in pregnancy: an evaluation using thromboelastography.

Amniotic fluid embolism is a rare obstetric complication. The exact pathogenesis of this syndrome remains unknown and significant controversy exists whether coagulopathy should always be present. We used thromboelastography to assess the effect of amniotic fluid on coagulation and platelet function in pregnant women. Different volumes of amniotic fluid (10-60 microl) were added to blood (330 microl) from pregnant women and thromboelastography variables determined. There were three important findings. R time, reflecting time to first clot formation, was significantly decreased with the addition of 10 microl amniotic fluid; platelet function, as determined by Reopro-TEG technique, was increased with the addition of 30 microl of amniotic fluid; and there was no evidence of fibrinolysis in any samples studied. In conclusion, our study substantiates the hypothesis that coagulation profile changes are invariable accompaniments of amniotic fluid embolism.

Adult↗
PubMed1983

Effects of dazoxiben on exercise performance in chronic stable angina.

1 We have performed a double-blind, randomized, 7-d cross-over study of the thromboxane synthetase inhibitor dazoxiben (UK 37248) in 20 patients with stable coronary heart disease. 2 All patients had a history of exertional angina of greater than two years duration and no patient had suffered a myocardial infarction in the preceding twelve months. 3 All patients had a positive exercise stress test for myocardial ischaemia and 15 had undergone coronary angiography. All these patients had a 50% narrowing in at least one vessel. 4 All patients were on conventional anti-anginal medication and the doses of their various therapies remained unchanged in the three months prior to and during the study period. 5 Therapy with dazoxiben 200 mg four times daily produced no alteration in the subjective or objective features of angina in these patients. There was no alteration in angina attack rate, glyceryl trinitrate consumption or duration of treadmill exercise. 6 Dazoxiben produced a highly significant reduction in both the resting and the post-exercise levels of serum thromboxane B2 levels, although there was no significant difference between the pre-exercise and post-exercise values. 7 Dazoxiben is an effective inhibitor of the synthesis of thromboxane but it has no effect on the subjective or objective features of stable coronary disease. This would suggest that the production of thromboxane and the development of circulating platelet aggregates play no part in the mechanism of angina in patients with stable coronary heart disease.

Angina Pectoris↗
PubMed2006

Global tests of haemostasis in critically ill patients with severe sepsis syndrome compared to controls.

Haemostatic changes in septic patients are complex, with both procoagulant and anticoagulant changes. Thirty-eight patients with severe sepsis and 32 controls were investigated by coagulation screens, individual factor assays, calibrated automated thrombography (CAT), whole blood low-dose-tissue factor activated (LD-TFA) Rotem and LD-TFA waveform analysis. Thirty-six of 38 patients had an abnormal coagulation screen. The mean levels of factors II, V (P < 0.05), VII, X, XI and XII, antithrombin and protein C (P < 0.01) was decreased in sepsis compared with controls. The mean factor VIII and fibrinogen level (P < 0.001) was increased. CAT in platelet rich and poor plasma showed a prolonged lag time (P < 0.02), decreased peak thrombin (P < 0.02) and delayed time to peak thrombin (P < 0.001) in sepsis patients, however, the endogenous thrombin potential was equivalent in sepsis and controls. In LD-TFA Rotem, septic patients had delayed clot times (P = 0.04) but an increased maximum velocity of clot formation (P < 0.01) and area under the clot elasticity curve (P < 0.01). LD-TFA waveform analysis showed a delayed onset time but an increased rate of clot formation (P < 0.005). In conclusion, global tests of haemostasis suggest that in this patient group, activation of haemostasis is delayed but once initiated thrombin generation and clot formation are normal or enhanced.

Adult↗