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PubMed2000

Effects of tranexamic acid and aprotinin, two antifibrinolytic drugs, on PAF-induced plasma extravasation in unanesthetized rats.

Two antifibrinolytic drugs, tranexamic acid (TXA), and aprotinin (APR), are currently used to improve the recovery of patients following major surgery while reducing blood loss. Their mechanisms of action have yet to be fully understood. Here, we examined (1) the effects of TXA or APR on basal vascular permeability (VP) and (2) the effects of TXA or APR on platelet-activating factor (PAF)-induced increase of VP in normal unanesthetized rats. Evans blue dye (EB) bound to albumin was used as the marker of extravasation in selected tissues. In normal rats, PAF (1 microg/kg i.v.) increased VP in most selected tissues including bronchi, aorta, duodenum and pancreas without affecting blood pressure. TXA (up to 300 mg/kg i.v.) had no significant effect on basal VP in any tissues, while APR (30000 KIU/kg i.v.) decreased basal VP in 5 out of 8 tissues. Pre-treatment with TXA decreased PAF-induced increases of VP in the microcirculation of the thoracic and abdominal aorta, the duodenum and the pancreas, from 35% to 41%. TXA was mostly effective at an i.v. dose of 100 mg/kg with a 2 h of pre-treatment period. Pre-treatment with APR also reduced PAF-induced increases of VP in selected tissues by 35 to 61%. The i.v. dose of 30000 KIU/mg was optimal when injected at least 30 min before the administration of PAF + Evans blue. These results suggest that the beneficial effect of APR and TXA, following cardiopulmonary bypass (CPB) and other type of surgeries, may be attributed to the inhibition of plasma exudation mediated, at least in part, by PAF. Thus, TXA and APR may improve patients recovery by reducing the capillary leakage of albumin, associated with interstitial edema formation, and maintaining intravascular fluid volume.

Animals↗
PubMed1998

The effect of three different doses of tranexamic acid on blood loss after cardiac surgery with mild systemic hypothermia (32 degrees C).

OBJECTIVE: Prophylactic administration of tranexamic acid (TA), an antifibrinolytic agent, decreases bleeding after cardiac surgery with systemic hypothermia (25 degrees C to 29 degrees C). Warmer systemic temperatures during cardiopulmonary bypass (CPB) may reduce bleeding and thus alter the requirement for TA. The effect of three different doses of TA on bleeding after cardiac surgery with mild systemic hypothermia (32 degrees C) is evaluated. DESIGN: Double-blind, prospective, randomized study. SETTING: University hospital. PARTICIPANTS: One hundred fifty adult patients undergoing aortocoronary bypass or valvular cardiac surgery. INTERVENTIONS: Patients received TA, 50 (n = 50), 100 (n = 50), or 150 (n = 50) mg/kg intravenously before CPB with mild systemic hypothermia. MEASUREMENTS AND MAIN RESULTS: Blood loss through chest drains over 6, 12, and 24 hours after surgery and total hemoglobin loss were measured. Autotransfused blood, transfused banked blood and blood products, and coagulation profiles were measured. Analysis of variance on log-transformed data for blood loss and confidence intervals (CIs) of 0.95 were calculated and transformed to milliliters of blood. No patient was re-explored for bleeding. Blood loss at 6 hours was statistically greater in the 50-mg/kg group compared with the other two groups (p = 0.03; p = 0.02). Total hemoglobin loss was statistically greater in the 50-mg/kg group compared with the 150-mg/kg group (p = 0.04). There was no statistical difference in blood tranfusion rate or coagulation profiles among the three groups. However, preoperative hemoglobin level was statistically lower in the 150-mg/kg group compared with the other two groups (p = 0.01). CONCLUSION: Of the three doses of TA studied, the most efficacious and cost-effective dose to reduce bleeding after cardiac surgery with mild hypothermic systemic perfusion is 100 mg/kg.

Adult↗
PubMed1976

Treatment of hereditary angioneurotic edema with tranexamic acid and cinnarizine.

Six out of 7 Finnish patients suffering from hereditary angioneurotic edema were helped during attacks, by treatment with tranexamic acid (AMCA, Cyklokapron, Kabi) in doses of 1.5 g 3 times daily, follow-up time 3-25 months. 3 of these patients also had continuous AMCA treatment, in the course of which 2 remained nearly symptom-free on a dosage of 1 g 2-3 times daily. Even the third one had shorter and milder attacks. One patient, however, had to stop taking AMCA after 6 weeks' treatment, because of fatigue and nausea. Follow-up time for the others was 9-11 months. For comparative purposes, 3 patients were given continuous treatment with an antihistamine, cinnarizine in a dosage of 20-30 mg daily. Two of the patients were helped by it, one becoming nearly symptom-free and the other having fewer and milder attacks; follow-up time 9-10 months.

Adult↗
PubMed2004

Role of fibrinolysis in tissue-factor-induced disseminated intravascular coagulation in rats - an effect of tranexamic acid.

We clarified the role of fibrinolysis in tissue-factor (TF)-induced rat disseminated intravascular coagulation (DIC) using tranexamic acid (TA). TA suppressed the elevation in D-dimer levels normally observed following TF-induced DIC, and an increase in organ dysfunction was seen. Enhanced fibrinolysis plays an important role in preventing the development of organ failure in TF-induced DIC.

Animals↗
PubMed1995

Does tranexamic acid reduce blood loss in knee arthroplasty?

In a retrospective study of 179 total knee arthroplasties, 70 patients received tranexamic acid (Cyklokapron, Kabi Pharmacia, Uppsala, Sweden) before the tourniquet was released to reduce postoperative blood loss. A group of 109 patients who underwent surgery before this treatment was introduced served as controls. Multiple regression analysis showed that the average postoperative blood loss was 340 mL less in treated patients compared with controls. Blood transfusions were reduced from 2 to 0 units (median values). Complications did not differ between the two groups apart from the number of postoperative hematomas.

Aged↗
PubMed1997

Use of tranexamic acid mouthwash to prevent postoperative bleeding in oral surgery patients on oral anticoagulant medication.

The clinical hemostatic effect of tranexamic acid mouthwash after oral surgery was evaluated in 47 patients receiving oral anticoagulant therapy. Surgery was performed after the anticoagulant medication was reduced in 15 patients (control group) and with no change in anticoagulant therapy in 32 patients (test group). The only statistical difference between the two treatment groups at baseline was the level of anticoagulation, which was significantly higher in the test group. There was no significant difference between the two treatment groups in the incidence of bleeding after oral surgery. The results indicated that a combination of local antifibrinolytic therapy and a local hemostatic agent is effective in preventing postoperative bleeding after oral surgery in patients treated with anticoagulants.

Administration, Oral↗
PubMed2001

[Clinical study on the efficacy of tranexamic acid in reducing postpartum blood lose: a randomized, comparative, multicenter trial].

OBJECTIVE: To study the efficacy and safety of Transamin (tranexamic acid) in reducing postpartum blood loss. METHODS: Four hundred primipara with term singleton pregnancy, vertex presentation, spontaneous delivery were enrolled. Ten U Oxytocin was injected intravenously immediately after the delivery of fetal shoulders in the second stage of labor. Then all the puerperants were randomly assigned to 4 groups. Group I (n = 94): Transamin 1.0 g was injected i.v.; Group lI (n = 92): Transamin 0.5 g i.v.; Group III (n = 92): aminomethylbenzoic acid 0.5 g i.v. was given; Group IV (n = 87): no treatment. Vaginal bleeding was precisely collected, and examined immediately after the expulsion of placenta and from placenta expulsion till 2 hours after delivery. The amount of blood loss was measured by both methods of weight and volume. RESULTS: There were no significant differences of blood loss immediately after the expulsion of placenta among the 4 groups (P > 0.05). For the average blood loss at 2 hour postpartum, it was 129.7 ml, 133.9 ml, 168.5 ml and 178.2 ml for group I, II, II and IV respectively, while the total blood loss for the 4 groups was 243.3 ml, 242.9 ml, 308.1 ml, and 314.8 ml respectively. The average blood loss of group I and II was significantly less than group III and IV (P < 0.01), however, there was no significant difference between group I and group II (P > 0.05). The occurrences of postpartum hemorrhage (blood lose > or = 400 ml) were 6.4%, 13.3%, 20.7% and 25.3% for group I, II, III and IV respectively. There was no major adverse effects appeared. CONCLUSIONS: Transamin is efficient and safe in reducing the postpartum blood loss. 1.0 g of Transamin has the best efficacy, and 0.5 g of Transamin followed.

Antifibrinolytic Agents↗
PubMed1980

Activation of factor XII in plasma from rats pretreated with tranexamic acid. Inhibition of a plasmin-induced loss of the functional activity of high molecular weight kininogen.

Incubation of plasma from rats pretreated with tranexamic acid (40 mg/100 g) with acetone (23% V/V) yielded enzyme preparations in which all the plasminogen present was recovered as plasmin and a plasmin-like substance without affinity for lysine-Sepharose. This substance, designated "plasmin", was separated from plasmin and kallikrein in a three-step procedure using columns of lysine-Sepharose, DEAE-Sephadex A-50, and arginine-Sepharose. The ratios of fibrinolytic, caseinolytic, LEe esterase, BAEe esterase and kininogenase activities of "plasmin" corresponded well with those of rat plasmin and human plasmin. Both rat plasmin and "plasmin" destroyed the capacity of high molecular weight kininogen (HMWK) to function as a cofactor in the activation of factor XII in rat plasma, without causing a corresponding release of the kinin part of the molecule. Rat plasma kallikrein induced full release of kinin from HMWK, but the functional capacity was retained. It is suggested that the reduced extent of activation of factor XII observed in plasma from rats injected intravenously with dextran, or rat plasma that has been passed through a column with lysine-Sepharose, is due to the loss of functional HMWK caused by plasmin activated in vivo or on the column.

Animals↗
PubMed1978

Secondary haemorrhage following traumatic hyphaema. A comparative study of conservative and tranexamic acid treatment.

Three out of 56 consecutively admitted patients with traumatic hyhaema, treated conservatively, developed secondary haemorrhage. Of the following 64 patients treated with tranexamic acid, none developed secondary haemorrhage. Statistical analysis, using chi2 test with Yate's correction showed no statistical difference with regard to the occurrence of secondary haemorrhage between the two groups.

Adolescent↗
PubMed1981

Determination of tranexamic acid (AMCA) and fibrin/fibrinogen degradation products in cerebrospinal fluid after aneurysmal subarachnoid haemorrhage.

Six patients with recently ruptured intracranial aneurysms were treated preoperatively with tranexamic acid (AMCA). Two patients received 6 g daily in i.v. infusion, two had 6 g daily by i.v. injection, and two patients were given AMCA 9 g daily by mouth during the first week after bleeding. Serial assays of AMCA and fibrin/fibrinogen degradation products (FDP) in cerebrospinal fluid (CSF) were performed during 6--13 days after the initial subarachnoid haemorrhage (SAH). Judged from the decline in CSF-FDP, an assumed therapeutic level of greater than or equal to 1 mg/l of AMCA in CSF was reached within 24--36 hours after the first dose when the drug was administered intravenously and within 48 hours when the drug was given orally.

Adult↗
PubMed1984

Inhibition of the late phase reaction to anti-human IgE in man by oral tranexamic acid.

Pharmacological modulation of the immediate and late phase reaction (LPR) to anti-human IgE was further investigated in a double-blind cross-over study. Tranexamic acid (AMCA) 1 g t.i.d. 24 h prior to and following intradermal injection of anti-IgE produced an approximate 40% inhibition of the LPR (P less than 0.01) without affecting the early response as compared with placebo in 10 volunteers. Antagonistic effect on activation of fibrinolysis and possibly the complement system is suggested as a possible mode of action.

Antibodies, Anti-Idiotypic↗
PubMed1972

Metabolism of plasminogen in healthy subjects: effect of tranexamic acid.

The metabolism of human plasminogen labeled with radioactive iodine was studied in 12 healthy men. The labeled plasminogen had a high specific activity and the same elution on Sephadex G-100 as the plasminogen activity in plasma. Immunoelectrophoresis revealed a single precipitin line. Polyacrylamide gel electrophoresis revealed six main bands, all with plasminogen properties and radioactivity. The purified plasminogen behaved as a homogeneous protein in the turnover experiments. The plasma radioactivity data were adequately approximated by a sum of two exponential terms. The metabolism of plasminogen was therefore represented by a two-compartment mammillary model. Results in the 12 normal subjects were as follows: plasma plasminogen concentration 20.8+/-1.9 mg/100 ml; intravascular plasminogen pool 0.66+/-0.14 g; intravascular fraction 0.59+/-0.06; fractional catabolic rate 0.55+/-0.09 of the plasma pool per day; half-life of the plasma radioactivity 2.21+/-0.29 days. Circulating large-molecular-weight degradation products of labeled plasminogen could not be detected by Sephadex G-100 gel filtration. The plasminogen turnover rate was normal in a patient with Behçet's syndrome and low circulating plasminogen activator activity. This finding supports the concept that under normal conditions the primary pathway of plasminogen catabolism is not via the formation of plasmin. The in vivo effect of tranexamic acid, a potent inhibitor of plasminogen activation, on the turnover of labeled plasminogen was studied in five normal subjects. When 1 g was administered perorally t.i.d. to three of them, one showed an increased plasminogen turnover. A 2 g dose administered t.i.d. to the other two caused markedly increased catabolism in both. This increase may be attributable to a direct reversible effect of tranexamic acid on the plasminogen molecule.

Acrylamides↗
PubMed1990

Tranexamic acid therapy in acute myeloid leukemia: possible reduction of platelet transfusions.

We studied the clinical efficacy and safety of the antifibrinolytic drug tranexamic acid (TA) in patients undergoing chemotherapy for acute leukemia. 54 newley diagnosed AML patients were treated with 1 g of TA every 6 hours until the platelet count rose to above 20 x 10(9)/l. Platelet transfusions were given, irrespective of the count, only when oral, mucosal or significant skin bleeding manifestations were observed. During induction, the average number of days with thrombocytopenia below 20 x 10(9)/l was 14.4 +/- 7.4 and 4.6 +/- 4.1 transfusions were given in each course. During consolidation, the average number of thrombocytopenic days was 8.4 +/- 8.5 and only 1.7 +/- 1.8 transfusions were administered. In 11.5% of the induction and 32.1% of the consolidation courses, no platelet support was required. TA was tolerated very well and no side effects or thromboembolic complications were observed. Only in 6 of the 78 induction courses did a major bleeding event occur and there were none in any of the 53 consolidation courses. Thus it seems that TA therapy allowed a significant reduction in the use of platelet transfusions without submitting the patients to greater bleeding risks.

Acute Disease↗
PubMed1970

Treatment of menorrhagia with tranexamic acid. A double-blind trial.

In a double-blind trial tranexamic acid (Cyclokapron) 1 g. four times a day for the first four days of menstruation, significantly decreased menstrual blood loss in women with menorrhagia for which no organic cause had been found. No difference in side-effects was noted between the active and placebo treatment.

Adult↗