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PubMed1994

Predictive factors of hyperfibrinolytic activity during liver transplantation in cirrhotic patients.

Hyperfibrinolytic activity occurs frequently during liver transplantation in cirrhotic patients. In order to identify those patients at high risk for increased intraoperative blood loss before operation, we determined predictive indicators of hyperfibrinolysis. We studied 56 cirrhotic patients undergoing liver transplantation with the same anaesthetic procedure and transfusion regimen. The preoperative coagulation patterns of the 11 patients who experienced acute intraoperative hyperfibrinolytic activity were compared with those of the 45 patients who did not suffer this complication. Before surgery, patients with intraoperative hyperfibrinolysis had decreased prothrombin time (PT) and euglobulin lysis time (ELT), and increased thrombin time (TT) and fibrinogen degradation products (FDP), whereas alpha angle and maximum amplitude (MA) were reduced on thrombelastography. Stepwise multivariate analysis disclosed three components which were significantly linked with occurrence of hyperfibrinolysis: TT, FDP and MA. Their sensitivity, specificity, positive and negative predictive values demonstrated that patients with FDP > or = 48 mg litre-1 and MA < or = 35 mm before incision had 100% probability of developing hyperfibrinolytic activity during transplantation.

Adult↗
PubMed1996

Lidocaine inhibits blood coagulation: implications for epidural blood patch.

Lidocaine in the epidural space, through inhibitory effects upon coagulation, may contribute to inefficacy of epidural autologous blood patch (EBP). This study was undertaken to evaluate the effect of achievable epidural concentrations of lidocaine on blood coagulation as a step in testing this hypothesis. Ex vivo blood coagulation using whole blood (n = 20) was studied with computerized thrombelastography (TEG). Each blood specimen was exposed to serial dilutions of lidocaine hydrochloride or saline to form end-concentrations of 0.0 mM, 2.3 mM, 4.6 mM, 9.2 mM, 18.5 mM, and 36.9 mM lidocaine. Statistical analysis using analysis of variance for repeated measures revealed that the three highest lidocaine concentrations tested caused hypocoagulable and/or fibrinolytic changes as compared with controls. Achievable epidural admixtures of lidocaine and whole blood will impair coagulation. Therefore, residual lidocaine in the epidural space may contribute to failures of immediate or early EBP.

Blood Coagulation↗
PubMed1993

Screening for fibrinolysis inhibitory effect of synthetic thrombin inhibitors.

Fibrin plate assay (FPA) and thrombelastography (TEG) were used to assess the antifibrinolytic effects of D-Phe-Pro-Arg-H (1), the prototype of peptide aldehyde inhibitors of thrombin, and two of its more stable derivatives, D-MePhe-Pro-Arg-H (2) and Boc-D-Phe-Pro-Arg-H (3). Inhibition of plasmin generation by tissue plasminogen activator, urokinase and streptokinase were studied by both FPA and TEG while that of plasmin could only be examined by FPA. TEG was more sensitive than FPA in general and for the detection of streptokinase inhibition in particular. Derivative (3) was 2-50 times more inhibitory than (1) or (2) depending on the enzyme studied and the assay system used. The thrombin selectivities of (1)-(3) were defined as the thrombin to fibrinolytic enzyme potency ratios. Data obtained by the FPA and thrombin time assay indicated (1) and (2) to be 2-80 times more selective for thrombin than (3). On the other hand, the values determined by TEG and recalcification assay showed the thrombin selectivity of (2) to be two to three times higher than that of (1), and (3) to have no such selectivity. According to TEG studies, (1) and (2) assisted rather than inhibited fibrinolysis by reducing the elasticity of human plasma clots.

Evaluation Studies as Topic↗
PubMed1998

Haemostatic disturbances in burned patients during early excision and skin grafting.

Bleeding is a major problem during early excision of burned skin. Therefore, 13 severely burned adult patients operated on during the first week after the trauma were studied. Blood loss was replaced with crystalloids, colloids and packed red cell concentrates (PRC). After ten infused PRCs, four fresh frozen plasma (FFP) units were given and thereafter one FFP unit with one PRC unit. Arterial blood samples were drawn before anaesthesia (SO), during operation after every four units of PRC transfusion (S1-4), 4 h postoperatively (S5) and on the first postoperative morning (S6). Prothrombin time (%) and activated partial thromboplastin time (s) were abnormal before operation (median values 67%, range 22-99% and 44 s, range 30-86 s, respectively). Prothrombin time decreased during operation and reached the critical level for normal haemostasis at S2. Thrombelastography showed decreased clot formation rate and impaired fibrin platelet interaction peri- and postoperatively. Fibrinogen and factor VIII activity were high preoperatively (median 6.1 g/l and 253%) and the critical values for normal haemostasis were not reached. Burned patients have a consumption coagulopathy which, in combination with haemodilution during operation, results in a clinically significant deficiency of coagulation factors II, VII and X, in spite of reactive elevation of coagulation factor VIII and fibrinogen.

Adult↗
PubMed2003

Effect of in vitro hemodilution with hydroxyethyl starch and dextran on the activity of plasma clotting factors.

OBJECTIVE: A recent thrombelastography study indicated a compromised in vitro blood coagulation after 10:10 (equal parts of blood and infusion) and 10:4 (10 parts blood to four parts infusion) hemodilution with several plasma substitutes. Oncovertin N (Oncovertin) (a 10% dextran 40 solution) had the strongest anticoagulant effect of all solutions tested, and HAES-sterile 10% (HAES) (a 10% hydroxyethyl starch 200/0.5 solution) showed the strongest effect of five different hydroxyethyl starch preparations. The aim of this study was to determine how in vitro hemodilution with HAES and Oncovertin affects the activity of coagulation factors. DESIGN: HAES and Oncovertin were tested to determine the intrinsic effect of colloid molecules, as opposed to hemodilution. Normal saline (NaCl) and nonlactated Ringer solution were used as noncolloidal controls. SETTING: University research institute. PATIENTS: Six healthy volunteers. INTERVENTIONS: Twenty milliliters of blood was obtained from each subject. MEASUREMENTS AND MAIN RESULTS: Prothrombin index, activated partial prothrombin time, soluble fibrin monomers, and the activity of coagulation factors I, II, V, VII, VIII, IX, X, XI, and XII were measured with the Behring Chromotimer according to the manufacturer's instructions. Two dilution ratios of citrated blood to infusion were used: 10:10 (equal parts of blood and infusion) and 10:4 (10 parts blood to four parts infusion). Baseline was undiluted. Hemodilution with NaCl at both 10:4 and 10:10 influenced the coagulation variables measured. The activities of factors I, VII, and soluble fibrin monomers were less influenced than expected by hemodilution alone. The activities of factors II, V, IX, and XI were significantly (p <.04) lower with both 10:4 and 10:10 dilution with NaCl. In the assays for factors IX, XI, and XII, clots formed immediately after adding the appropriate reagents in the presence of Ringer solution at 10:10 hemodilution, so that the activities of those factors could not be measured. For the other factors and for 10:4 dilution, the outcome after Ringer solution was similar to that of NaCl. The activities were less influenced after 10:4 hemodilution with both HAES and Oncovertin than after dilution with NaCl and Ringer solution, with no significant differences from baseline. At 10:10 hemodilution with both HAES and Oncovertin, several factor activities were significantly (p <.04) lower than baseline. CONCLUSIONS: Both NaCl and Ringer solution cause measurable effects on coagulation factors at 10:4 hemodilution that can be explained by hemodilution alone. The effects on clotting factors of 10:4 hemodilution with HAES and Oncovertin were not significant. Even at 10:10 hemodilution with HAES or Oncovertin, the reduction in factor activities, although significantly (p <.04) different from baseline, was less than what was expected by dilution alone.

Blood Coagulation Factors↗
PubMed1989

Systemic effects of tissue plasminogen activator-associated fibrinolysis and its relation to thrombin generation in orthotopic liver transplantation.

Orthotopic liver transplantation is frequently associated with hyperfibrinolysis, the origin and clinical relevance of which is largely unknown. In 20 orthotopic liver transplantations, we studied the occurrence and systemic effects of hyperfibrinolysis. Severe fibrinolysis was defined to be present when the euglobulin-clot lysis time and the whole-blood-clot lysis time, as measured by thrombelastography, were shorter than 60 and 90 min, respectively, at some time during the operation. Based on these criteria, 7 patients had minimal fibrinolysis (group I), and 13 patients had severe fibrinolysis (group II). In group II a gradual increase of tissue-type plasminogen activator (t-PA) activity was seen during the anhepatic stage, followed by an "explosive" increase immediately after graft reperfusion (P = 0.0004, compared with group I), and a reduction of plasminogen activator inhibitor (PAI) activity. Plasma degradation products of fibrinogen and fibrin increased parallel to t-PA activity, and levels were significantly higher at 45 min after graft reperfusion in group II compared with group I (P less than 0.04). Thrombin-antithrombin III complexes showed an identical steady increase in both groups, indicating that increased t-PA activity was not related to thrombin formation. A combination of increased endothelial release and reduced hepatic clearance may have caused the increased t-PA activity. The t-PA-associated destruction of fibrinogen and fibrin after graft reperfusion is consistent with the clinical signs of severe oozing often seen in this period. These observations may have important clinical implications for the treatment of bleeding in patients undergoing orthotopic liver transplantation.

Adult↗
PubMed1992

Different aprotinin applications influencing hemostatic changes in orthotopic liver transplantation.

The effect of different aprotinin applications on hemostatic changes and blood product requirements in orthotopic liver transplantation was investigated in a prospective, open, and randomized study. From November 1989 to June 1990, 13 patients received aprotinin as a bolus of 0.5 Mill. Kallikrein inactivator units (KIU) on three occasions in the course of an OLT, whereas 10 other patients were treated with continuous aprotinin infusion of 0.1-0.4 Mill. KIU/hr. Before and after reperfusion of the graft liver, signs of hyperfibrinolysis, measured by thrombelastography, were significantly lower in the infusion group. Tissue-type plasminogen activator (t-PA) activity increased during the anhepatic phase but to a significantly lesser extent in the infusion group. Blood product requirements during OLT were tendentiously higher in the bolus group but not significantly so. However, the use of packed red blood cells was significantly lower in the postoperative period, whereas there was no significant difference in fresh frozen plasma requirements between the two groups. All 23 patients have survived, and only one woman of each group required retransplantation due to severe host-versus-graft reactions. Furthermore, we investigated the perfusate of the graft liver in both groups and detected signs of a decreased t-PA release in the infusion group. Our results demonstrate an advantage of aprotinin given as continuous infusion over bolus application in OLT.

Aprotinin↗
PubMed2002

Coagulopathy mediated by hepatoenteric ischemia-reperfusion in rabbits: role of xanthine oxidase.

Hepatic transplantation may result in coagulopathy caused by the release of mast-cell-derived heparin, and xanthine oxidase (XO) inhibition stabilizes mast cells. Thus, XO inactivation could decrease coagulopathy after hepatoenteric ischemia-reperfusion. Rabbits were fed a standard or XO-inactivating diet before hepatoenteric ischemia for 35 min and before 30 min of reperfusion. Hemostasis was assessed by thrombelastography. Heparin activity was quantified by anti-IIa. XO inactivation resulted in clot formation after reperfusion in all animals, whereas only 37.5% of animals with XO activity clotted (P<0.05). Anti-IIa activity was less in animals at baseline and after reperfusion with XO inactivation (45+/-5 and 65+/-5 mU/mL, respectively) compared to animals with XO activity (51+/-4 and 71+/-5 mU/mL, respectively) (P<0.05). Clot strength, which was mediated by coagulation proteins, was significantly greater at baseline and after reperfusion in animals with XO inactivation. XO inactivation enhances hemostasis by decreasing circulating heparin activity and increasing coagulation protein function before ischemia-reperfusion.

Animals↗
PubMed2007

Hydroxyethyl starch enhances argatroban-mediated decreases in clot propagation and strength by diminishing thrombin-fibrinogen interactions.

Direct thrombin inhibitors (DTIs) have been administered for anticoagulation during cardiopulmonary bypass for patients with heparin-induced thrombocytopenia. While DTIs prolonged clot initiation and decreased clot propagation, clot strength did not change. Hydroxyethyl starches (HES), however, significantly decreased clot propagation and strength. We hypothesized that DTI with HES could significantly decrease hemostasis more than DTI alone. Plasma was exposed to 0 or 5 microg/ml argatroban with 0 or 30% dilution with 0.9% NaCl, 10% pentastarch or 6% Voluven. Additional argatroban-exposed samples diluted with HES had addition of alpha-thrombin (0.25 U/ml) and fibrinogen (150 mg/ml). Clot kinetics were determined via thrombelastography. While dilution with 0.9% NaCl significantly (P < 0.05) decreased the clot strength by 17% compared with samples only exposed to argatroban, dilution with pentastarch and Voluven significantly (P < 0.05) markedly decreased clot strength (53 and 78%, respectively). Voluven dilution significantly increased the time to clot initiation and decreased the velocity of clot propagation compared with samples only exposed to argatroban. Addition of alpha-thrombin/fibrinogen restored clot strength. DTI/HES administration diminished hemostasis to a greater extent than DTI exposure alone. Further investigation is warranted to determine whether this therapeutic approach can improve the safety of anticoagulation during cardiopulmonary bypass in patients with heparin-induced thrombocytopenia.

Anticoagulants↗
PubMed1975

Changes in blood catecholamine levels and blood coagulation and fibrinolytic activity in response to graded exercise in man.

Measurements of catecholamines, fibrinogen, factor VIII, thrombelastography, euglobulin lysis time and platelet adhesiveness have been carried out on venous blood obtained from normal males exposed to exercise on a bicycle ergometer at various work loads. Significant increases in adrenaline, factor VIII and fibrinogen were found only after exercise to exhaustion at 1500 kpm min-1 whereas the euglobulin lysis time was inversely proportional to the excercise load. There was no change in platelet adhesiveness. These findings support the results of studies using adrenaline infusions or adrenergic blockade which suggest that stress-induced increases in factor VIII are mediated via adrenergic stimulation but that activation of fibrinolysis is not dependent on adrenaline.

Adult↗
PubMed2004

Unresponsiveness to factor VIII inhibitor bypassing agents during haemostatic treatment for life-threatening massive bleeding in a patient with haemophilia A and a high responding inhibitor.

We report a case of haemophilia A with a high responding inhibitor of factor VIII (FVIII) who had a serious retroperitoneal haematoma caused by penetration of a duodenal ulcer. Inhibitor-bypassing therapy was commenced immediately on admission. On the 17th day of treatment with activated prothrombin complex concentrate (APCC; FEIBA, re-bleeding occurred and thrombelastography (TEG) demonstrated resistance to therapy. Treatment was changed to recombinant activated factor VII (rFVIIa; NovoSeven and resulted in clinical improvement together with an improvement in TEG parameters. On the 10th day of continuous infusion with NovoSeven, however, TEG again showed resistance to therapy. FEIBA infusions were re-introduced and TEG results remained satisfactory for 7 days. On day 34, however, further retroperitoneal bleeding was evident and a decline in the haemostatic efficiency of FEIBA was recorded by TEG. NovoSeven was again successfully administered for 7 days. There were no laboratory findings to indicate disseminated intravascular coagulation (DIC), hypercoagulability or abnormal fibrinolysis. The plasma-based clotting tests did not show any additional prolongation on the occasions when the TEG demonstrated unresponsiveness to FEIBA or NovoSeven. These findings suggested that some component of whole blood, other than plasma might have governed the TEG data. The long-term use of APCC such as FEIBA or rFVIIa, requires careful monitoring in terms of FVIII inhibitor bypassing activity as well as the tendency to DIC.

Adolescent↗
PubMed2006

New approaches for measuring coagulation.

Although specific assays of coagulation factors are essential for diagnostic purposes they only give partial information about an individual's haemostatic state. This can be better assessed by various global tests, and recent developments and evaluations of five such tests are described in this symposium: the PFA-100; waveform analysis; thrombin generation; overall haemostasis potential; thrombelastography. Each test has advantages in various applications, but the thrombin generation test and waveform analysis have been found most useful in haemophilia, whilst the PFA-100 is helpful in von Willebrand's disease.

Blood Coagulation Disorders↗
PubMed1998

Hydroxyethyl starch impairs in vitro coagulation.

BACKGROUND: Artificial colloids affect haemostasis. Particularly hydroxyethyl starch (HES) solutions may have detrimental effects on haemostatic mechanisms. METHODS: In a crossover study blood was withdrawn from ten volunteers. Ringer's acetate, 6% low molecular weight HES (MW 120,000/molar substitution ratio 0.7), 10% low molecular weight HES MW 200,000/0.5) and 6% high molecular weight HES (MW 400,000/0.7) or 4% albumin was added to venous blood samples to make either 20 vol.% or 50 vol.% concentrations of each of the solutions. Samples were analyzed by thrombelastography (TEG). RESULTS: All HES solutions at 20 vol.% concentration impaired haemostasis as demonstrated by decreased clot formation rate (alpha-angle and maximum amplitude (MA)). In contrast, Ringer's acetate and albumin improved coagulability at 20 vol.% concentrations. Coagulation time (r + K) was prolonged at 50 vol.% dilutions of all solutions. The median r + K was greater with HES 400 (P < 0.05) and HES 200 (N.S.) than with HES 120. CONCLUSION: We conclude that HES at 20 and 50 vol.% concentrations has an adverse effect on in vitro measures of coagulation. A 50% dilution with high molecular weight HES seems to impair coagulation more than low molecular weight HES. Ringer's acetate and albumin caused a hypercoagulable state at a concentration of 20 vol.%, but the higher concentration decreased coagulability.

Adult↗
PubMed1998

Preeclampsia: haemostatic status and the short-term effects of methyldopa and isradipine therapy.

OBJECTIVE: To determine the haemostatic status in preeclampsia and to investigate the effects of short-term use of anti-hypertensive drugs, methyldopa and isradipine. METHODS: Thirty preeclamptic (PE) women admitted to the hospital for observation and treatment were randomized to receive either methyldopa or isradipine for 2 weeks. Their blood pressure were monitored for 24 h before treatment and again at 7 days and 14 days after treatment using the programmable automated ambulatory blood pressure (ABP) monitoring system. Blood sampling was performed before commencement of anti-hypertensive treatment, 7 days and 14 days after treatment and the haemostatic parameters studied was compared before treatment with normal pregnancy and the effect of anti-hypertensive treatment. Nineteen normal pregnant subjects with a total of 30 blood sampling at various gestation and good pregnancy outcome served as controls. The following haemostatic parameters were determined; thrombelastography, fibrinogen, antithrombin III (ATIII), thrombin-antithrombin (TAT)-complex, beta-thromboglobulin (beta-TG), plasminogen activators (t-PA, u-PA), plasminogen activator inhibitors (PAI-1, PAI-2), and plasminogen. RESULTS: Significant lowering of blood pressure was evident at Days 7 and 14 of therapy with either methyldopa or isradipine. Increased mean plasma fibrinogen and decreased ATIII levels were seen in preeclampsia together with decreased u-PA and t-PA activity levels in contrast to increased t-PA antigen and beta-TG. No significant differences were seen for TAT-complex, PAI-1, plasminogen and D-dimer levels although their mean levels were higher than observed in non-pregnant subject except for PAI-2, the level was significantly reduced when compared with normal pregnancy. Two-way analysis of variance showed no significant alteration on all haemostatic parameters studied in preeclamptic women receiving either methyldopa or isradipine after 7 and 14 days of therapy. CONCLUSION: Enhance activation of coagulation was observed together with raised fibrinolysis in normal pregnancy and PE. However, in PE a further reduction in ATIII, u-PA and PAI-2 with increased fibrinogen and platelet activation could lead to an imbalance in the coagulation/fibrinolysis equilibrium which favours fibrin deposition. All these changes seen in PE including the coagulation kinetics were not altered by the short term effects of methyldopa and isradipine even though significantly lowered blood pressure were observed during therapy.

Antihypertensive Agents↗
PubMed1999

The FVII activating protease cleaves single-chain plasminogen activators.

A serine protease isolated from plasma sharing structural characteristics with a hepatocyte growth factor activator-like protease has been demonstrated recently to activate FVII. Accordingly, it was named 'FVII activator'. Until now an impact of this protease on the fibrinolytic system has not been reported. We islolated the protease from cryo-poor plasma by subsequent ion exchange chromatography and adsorption to immobilized heparin and/or aprotinin. Incubation of single-chain plasminogen activators (sc-PAs) with the FVII activator revealed significant activation of urokinase sc-PA (scu-PA) and tissue sc-PA (sct-PA) in vitro. It was enhanced in the presence of calcium and heparin. Compared to kallikrein, a more efficient activation of scu-PA was observed, whereas sct-PA appeared to be a poorer substrate for the FVI activator. At low protease concentrations and in the presence of heparin the scu-PA activation was comparable to plasmin. Employing recalcified whole blood thrombelastography, the lysis of initially formed fibrin was observed after addition of a combination of scu-PA and the FVII activator, whereas the scu-PA alone had a negligible effect at the concentration used. The study results as presented demonstrate that the FVII activator is a potent activator of sc-PAs in vitro. Whether it plays a physiological role in fibrinolysis deserves further investigation. Its comparatively high affinity to heparin assumes a function in cell surface or matrix events.

Blood Coagulation Factors↗
PubMed1978

Thrombocytopenia and coagulation impairment after portacaval shunt in the rat.

A study has been performed to evaluate the effect of the portacaval shunt on some coagulation tests in the rats. Thrombocytopenia develops, accompanied by a decrease in the total protein and fibrinogen concentrations. Moreover, the Quick time is lengthened, whereas the partial thromboplastin time is not modified. The maximal amplitude and elasticity of the clot, recorded by thrombelastography, appear reduced, and k is lengthened. The results are discussed.

Animals↗
PubMed2003

Inhibition of tumor cell-induced platelet aggregation and lung metastasis by the oral GpIIb/IIIa antagonist XV454.

Platelets are known to play a role in blood borne metastasis. Previous experimental studies have suggested that platelet GpIIb/IIIa may be a therapeutic target. However, the need for intravenous administration limits the potential application of current GpIIb/IIIa inhibitors to cancer therapy. The aim of the present study was to assess the efficacy of a novel, non-peptide oral GpIIb/IIIa antagonist (XV454) on tumor cell-induced platelet aggregation in vivo and on experimental metastasis. A Lewis lung carcinoma (LL2) mouse model of experimental metastasis was used in this study. XV454 (100 micro g) was administered intravenously (via tail vein) or orally (gavages) to 20 g mice. To determine the effect of XV454 on platelet aggregation, blood samples were collected by cardiac puncture 10 minutes after intravenous and 1-24 hrs after oral XV454, and platelet function was assessed by aggregometry, thrombelastography and the Platelet Function Analyzer (PFA100). The effect of XV454 on tumor cell-induced thrombocytopenia was determined 10 minutes after intravenous and 3 hrs after oral XV454 administration. Tumor cells (2 x 10(6)) were injected intravenously and 15 minutes after cell injection, platelet count was measured and compared to baseline (pre-injection) counts. To assess the effect on metastasis, XV454 was administered intravenous or orally 10 minutes and 3 hrs before tumor cell injection, respectively. Eighteen days later, surface lung tumor nodules were counted and the total lung tumor burden assessed. In a fourth group, in addition to the initial oral dose (before tumor cell injection), oral XV454 was given daily for the first week and three times in the second week. Administration of XV454 (5 mg/kg) completely inhibited platelet aggregation and this effect persisted for at least 24 hrs after oral delivery. Both intravenous and oral XV454 significantly inhibited tumor cell-induced thrombocytopenia (P < 0.01), the number of surface lung tumor nodules (80-85%; P < 0.001) and total tumor burden (83% for intravenous group; 50% oral [single treatment] group; 91% oral [multiple treatment] group, P < 0.001). Overall, these data provide further evidence for the effect of oral and intravenous GpIIb/IIIa antagonism on tumor cell-platelet interaction and metastasis.

Administration, Oral↗
PubMed2003

The effects of a one unit blood donation on auto-haemodilution and coagulation.

The effect of haemodilution on coagulation has been extensively investigated. We investigated auto-haemodilution following a 10% blood loss (480 ml) and its effect on coagulation. Ten healthy, unstarved volunteers were enrolled. One unit of blood was taken from each volunteer. Concurrently blood was taken from the opposite arm prior to and immediately after the blood donation, and at 1, 2, 4 and 6 hours. It was tested for thrombelastography, haematocrit and endorphins. There was a significant decrease in r-time from the control sample to the sample taken immediately post blood donation. This value returned to baseline at 1 hour post donation and did not change again. There were no other significant changes in thromboelastographic parameters. Fractional plasma noradrenaline changes were significantly raised at 1 hour post donation (P = 0.048), returning to baseline by 2 hours post donation. The haematocrit showed a rapid (approximately 4%) fall during donation followed by a slow, but progressive decrease over six hours, falling by a mean of 8.3% from pre-donation values. A state of relative hypercoagulability is found immediately after a rapid 10% loss in circulating blood volume. This may be related to the rapid immediate haemodilution. It is unlikely that the sympathetic response to blood loss plays a role. However, after the initial drop, slow restoration of circulating blood volume by autodilution takes six to eight hours, and is not associated with enhanced coagulation. Of interest is that a 10% blood loss in a healthy person does not require volume replacement.

Antithrombin III↗