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PubMed2002

Tranexamic acid, a widely used antifibrinolytic agent, causes convulsions by a gamma-aminobutyric acid(A) receptor antagonistic effect.

Application of 4-(aminomethyl)cyclohexanecarboxylic acid (tranexamic acid; TAMCA) to the central nervous system (CNS) has been shown to result in hyperexcitability and convulsions. However, the mechanisms underlying this action are unknown. In the present study, we demonstrate that TAMCA binds to the gamma-aminobutyric acid (GABA) binding site of GABA(A) receptors in membranes from rat cerebral cortex and does not interfere with N-methyl-D-aspartate receptors. Patch-clamp studies using human embryonic kidney cells transiently transfected with recombinant GABA(A) receptors composed of alpha 1 beta 2 gamma 2 subunits showed that TAMCA did not activate these receptors but dose dependently blocked GABA-induced chloride ion flux with an IC(50) of 7.1 +/- 3.1 mM. Application of TAMCA to the lumbar spinal cord of rats resulted in dose-dependent hyperexcitability, which was completely blocked by coapplication of the GABA(A) receptor agonist muscimol. These results indicate that TAMCA may induce hyperexcitability by blocking GABA-driven inhibition of the CNS.

Animals↗
PubMed1975

Patho-physiological studies on lactic acid-induced pulmonary thrombosis in rat. I. Effect of heparin, acetylsalicylic acid, urokinase and tranexamic acid.

The role of platelet aggregation and coagulo-fibrinolytic systems in thrombogenesis of lactic acid-induced pulmonary thrombosis in rat were studied using an anti-coagulant, platelet aggregation inhibitor, fibrinolytic or anti-fibrinolytic agents. In normal rat, heparin (2.5 mg/kg), acetylsalicylic acid (30 mg/kg) and tranexamic acid (100 mg/kg) suppressed specifically coagulation, platelet aggregation induced by collagen or thrombin and fibrinolysis respectively. Urokinase (10,000 units/kg) activated powerfully fibrinolytic system in addition to suppressing slightly platelet aggregation. The pretreatment with heparin, acetylsalicylic acid or urokinase markedly prevented the formation of thrombus initiated by the infusion of lactic acid at the doses used. Additive effect was also obtained by combined administration of these agents. On the other hand, it was interesting to note that tranexamic acid (100 mg/kg) did not affect the thrombus formation at all despite a potent anti-fibrinolytic effect of this agent. These results indicate that both platelet aggregation and enhancement of coagulation activity are important factors responsible for the formation of thrombi in DIC, while the fibrinolytic activity in blood seems not to be involved in it. On the basis of the findings, mechanism for triggering activation of coagulation and platelet aggregation is also discussed here.

Animals↗
PubMed1996

Changes in coagulation patterns, blood loss and blood use after cardiopulmonary bypass: aprotinin vs tranexamic acid vs epsilon aminocaproic acid.

Cardiopulmonary bypass (CPB) increases risk of postoperative bleeding and need for transfusion. The aim of this study was to evaluate the effects of aprotinin, epsilon aminocaproic acid and tranexamic acid on coagulation patterns and need for banked blood transfusion. Ninety-six consecutive patients who underwent coronary artery bypass surgery were randomly assigned to 4 groups (24 patients each). The following parameters were monitored before, during and after CPB: activated lotting time, hemoglobin, prothrombin time, activated prothromboplastin time, fibrinogen, antithrombin III, xDP, Factor VIII, Thrombin-Antithrombin Complex and plasminogen. Analysis of postoperative bleeding and need for transfusion showed that the aprotinin group had significantly lower mediastinal bleeding. Transfused patients were 2, 4, 12 and 18 respectively in the aprotinin, epsilon aminocaproic acid, tranexamic acid and placebo treated group. In conclusion the use of protease inhibitors significantly reduces postoperative bleeding and transfusion. The aprotinin-treated group had the lower need for transfusion.

Aminocaproic Acid↗
PubMed2006

A randomized trial of tranexamic acid in combination with cell salvage plus a meta-analysis of randomized trials evaluating tranexamic acid in off-pump coronary artery bypass grafting.

OBJECTIVES: We sought to evaluate the effectiveness of tranexamic acid in off-pump coronary artery bypass grafting surgery, either when used in combination with mechanical cell salvage or when used alone. METHODS: One hundred patients were randomized to either 2 g of tranexamic acid as an intravenous bolus before sternotomy or to placebo. Intraoperative and postoperative cell salvage was used in all patients. The primary end point was early postoperative blood loss (within 4 hours). To evaluate the efficacy of tranexamic acid in isolation, we also performed a meta-analysis of 4 randomized trials identified from a systematic literature search. The primary end point of the meta-analysis was red cell transfusion. RESULTS: In our randomized trial patients in the tranexamic acid group had a significant reduction in early postoperative blood loss, (median difference, 50 mL; 95% confidence interval, 15-100 mL; P < .01); however, there was no reduction in the frequency of blood component transfusion. Patients in the placebo group received a significantly larger volume of autotransfused red cells (median difference, 120 mL; 95% confidence interval, 0-220 mL; P = .02). The meta-analysis demonstrated a significant reduction in red cell transfusions in patients receiving tranexamic acid compared with those receiving placebo (risk ratio, 0.48; 95% confidence interval, 0.24-0.97; P = .041). There was also a reduction in the frequency of any allogeneic blood component transfusion, as well as a highly significant reduction in postoperative blood loss, in patients receiving tranexamic acid (P < .001). CONCLUSIONS: Tranexamic acid reduces blood loss and transfusion requirements in off-pump coronary artery bypass grafting surgery. A reduction in allogeneic blood transfusion was not evident in the presence of perioperative cell salvage. These data support the routine use of tranexamic acid in off-pump coronary artery bypass grafting surgery.

Adult↗
PubMed1990

Interactions of saruplase with acetylsalicylic acid, heparin, glyceryl trinitrate, tranexamic acid and aprotinin in a rabbit pulmonary thrombosis model.

In anesthetized rabbits with pulmonary embolized thrombi the interactions of saruplase (recombinant unglycosylated single-chain urokinase-type plasminogen activator, CAS 99149-95-8) with acetylsalicylic acid (ASA), glyceryl trinitrate (nitroglycerin, GTN), heparin, and the antifibrinolytics tranexamic acid and aprotinin have been studied. Lysis rates were evaluated as reduction of the weight and as reduction of the incorporated 125J-fibrin content of the embolized thrombi. In untreated controls the spontaneous 125J-fibrinolysis was 8.3 +/- 0.7% and the thrombus weight was reduced by 55.3 +/- 4.5% (mainly due to loss of H2O) at 195 min after the thromboembolization. Infusion of saruplase (21.5 micrograms/kg.min) for 60 min significantly increased the 125J-fibrinolysis to 36.8 +/- 3.7% and the reduction of the thrombus weight to 69.9 +/- 2.1%. ASA (50 mg/kg p.o.) by itself did not exert a lytic effect; in combination with saruplase ASA insignificantly augmented the 125J-fibrinolysis rate and significantly further increased the thrombus weight reduction. GTN (5.0 micrograms/kg.min i.v.) neither influenced the spontaneous nor the saruplase-mediated lysis rates. Treatment with heparin (200 IU/kg i.v.-bolus plus 50 IU/kg.min i.v.-infusion) resulted in significant greater thrombus weight reduction than observed in untreated controls; in combination with saruplase heparin significantly intensified the lytic effect. Tranexamic acid (30 mg/kg i.v.) and aprotinin (30.10(3) KIU/kg i.v.) completely abrogated the lytic effect of saruplase. Treatment with saruplase alone produced an insignificant decrease of the plasma level of fibrinogen by 23% to 200 +/- 20 mg/dl. ASA, GTN and aprotinin did not influence this slight fibrinogenolysis in saruplase-treated animals. A slight decrease of plasma fibrinogen levels was observed by heparin, whereas the decrease by tranexamic acid was significant.

Animals↗
PubMed1998

Prophylactic tranexamic acid and epsilon-aminocaproic acid for primary myocardial revascularization.

BACKGROUND: The efficacy of prophylactic epsilon-aminocaproic acid and tranexamic acid to reduce transfusions after primary myocardial revascularization was evaluated in a teaching hospital context. METHODS: Patients (n = 134) received either epsilon-aminocaproic acid (15-g bolus + infusion of 1 g/h), high-dose tranexamic acid (10-g bolus + placebo infusion), or normal saline solution in a double-blind fashion. Anticoagulation and conduct of cardiopulmonary bypass were standardized. RESULTS: Tranexamic acid and epsilon-aminocaproic acid produced a significant reduction in postoperative blood loss compared with placebo (median loss, 438 mL, 538 mL, and 700 mL, respectively). Transfusion of red cells was similar in all three groups. Nonetheless, the percentage of patients receiving hemostatic blood products was significantly decreased in the epsilon-aminocaproic acid group compared with the placebo group (20% versus 43%; p = 0.03). Both tranexamic acid and epsilon-aminocaproic acid significantly decreased total exposure to allogeneic blood products compared with placebo (p = 0.01 and p = 0.05, respectively), and this reduction was clinically important (median exposure, 2, 2, and 7.5 units, respectively). Fibrinolysis was inhibited significantly in both treatment groups. CONCLUSIONS: We conclude that either high-dose tranexamic acid or epsilon-aminocaproic acid effectively reduces transfusions in patients undergoing primary, elective myocardial revascularization.

Aminocaproic Acid↗
PubMed2000

Tranexamic acid reduces red cell transfusion better than epsilon-aminocaproic acid or placebo in liver transplantation.

UNLABELLED: We evaluated the efficacy of the prophylactic administration of epsilon-aminocaproic acid and tranexamic acid for reducing blood product requirements in orthotopic liver transplantation (OLT) in a prospective, double-blinded study performed in 132 consecutive patients. Patients were randomized to three groups and given one of three drugs prophylactically: tranexamic acid, 10 mg. kg(-1). h(-1); epsilon-aminocaproic acid, 16 mg. kg(-1). h(-1), and placebo (isotonic saline). Perioperative management was standardized. Coagulation tests, thromboelastogram, and blood requirements were recorded during OLT and in the first 24 h. There were no differences in diagnosis, Child score, or preoperative coagulation tests among groups. Administration of packed red blood cells was significantly reduced (P = 0.023) during OLT in the tranexamic acid group, but not in the epsilon-aminocaproic acid group. There were no differences in transfusion requirements after OLT. Thromboembolic events, reoperations, and mortality were similar in the three groups. Prophylactic administration of tranexamic acid, but not epsilon-aminocaproic acid, significantly reduces total packed red blood cell usage during OLT. IMPLICATIONS: In a randomized study of 132 consecutive patients undergoing liver transplantation, we found that tranexamic acid, but not epsilon-aminocaproic acid, reduced intraoperative total packed red blood cell transfusion.

Adult↗
PubMed1979

Tranexamic acid and corneal deturgescence.

Recent work has demonstrated decreased corneal thickness in patients with Fuch's dystrophy and in patients following cataract extraction who were given systemic acid. Although tranexamic acid is a known antifibrinolytic drug its mechanism in reducing corneal thickness is not known. This experiment demonstrated no increase in the rate of corneal deturgescence of swollen rabbit corneas in the specular microscope when they were perfused for three h with 1 mM or 10 mM tranexamic acid. Pre-treatment of rabbits with intravenous tranexamic acid for three days and subsequent perfusion of corneas with tranexamic acid 10 mM also did not increase the rate of corneal deturgescence when compared with controls.

Animals↗
PubMed1975

Plasminogen-plasmin system IX. Specific binding of tranexamic acid to plasmin.

Interactions between tranexamic acid and protein were studied in respect of the antifibrinolytic actions of tranexamic acid. Tranexamic acid did neither show any interaction with fibrinogen or fibrin, nor was incorporated into cross-linked fibrin structure by the action of factor XIII. On the other hand, tranexamic acid bound to human plasmin with a dissociation constant of 3.5 X 10-5 M, which was very close to the inhibition constatn (3.6 X 10-5 M1 for this compound in inhibiting plasmin-induced fibrinolysis. The binding site of tranexamic acid on plasmin was not the catalytic site of plasmin, because TLCK-blocked plasmin also showed a similar affinity to tranexamic acid (the dissociation constant, 2.9-4.8 x 10-5m). in the binding studies with the highly purified plasminogen and TLCK-plasmin preparations which were obtained by affinity chromatography on lysine-substituted Sepharose, the molar binding ratio was shown to be 1.5-1.6 moles tranexamic acid per one mole protein. On the basis of these and other findings, a model for the inhibitory mechanism of tranexamic acid is presented.

Antifibrinolytic Agents↗
PubMedDate not supplied

Tranexamic acid in oncology.

Tranexamic acid has the potential to be a pharmacologic adjunct for the prophylaxis of hemorrhagic complications occurring in the oncology population. The studies and cases reviewed here suggest that tranexamic acid administration may be a therapeutic option for bleeding prophylaxis in APL where enhanced fibrinolysis accompanies the disease state. Because of the lack of a control in these reports, and the small sample size, it is not possible to extrapolate these conclusions regarding the efficacy of tranexamic acid in preventing hemorrhage in the larger thrombocytopenic oncology population. However, these reports concluded that its administration is safe, with few adverse effects and no thromboembolic events noted. A large, well-designed, controlled clinical trial is needed before a recommendation for the routine use of tranexamic acid in the oncology population can be established.

Antifibrinolytic Agents↗
PubMed1994

Studies on the mechanisms of action of aprotinin and tranexamic acid as plasmin inhibitors and antifibrinolytic agents.

Both aprotinin and tranexamic acid are effective inhibitors of fibrinolysis in vitro and in vivo and both agents can act as plasmin inhibitors in purified systems, although there is some debate on their exact mechanism of action in vivo. The studies reported here using an in vitro clot lysis system designed to provide precise inhibition constants show that aprotinin remains a very potent inhibitor of plasmin even in the presence of fibrin with Ki = 2 nM. Plasmin-aprotinin interactions in solution are not affected by a number of kringle binding ligands, aminohexanoic acid, tranexamic acid or CNBr-fibrinogen fragments with Ki = 0.4 nM. The difference between these two Ki values is explained by competition for the plasmin active site between substrate (fibrin) and inhibitor (aprotinin). Inhibition of fibrinolysis by tranexamic acid is not readily analysed by a simple inhibition model which may be due to multiple overlapping ligand-kringle interactions or tranexamic-fibrin interactions. Experiments using combinations of aprotinin and tranexamic acid in the clot lysis system confirm the complementary nature of inhibitory mechanisms and suggest a slight synergism. These results support the idea that aprotinin inhibition of plasmin is a primary mode of action in vivo, and suggest that combination therapy of aprotinin with tranexamic acid might be more effective than either inhibitor alone.

Amino Acid Sequence↗
PubMed1976

Failure of tranexamic acid to influence the ellagic acid-induced hypercoagulable state.

Tranexamic acid in a dose of 50 mg/kg b.w. was unable to alter the ellagic acid induced hypercoagulable state. No change in the hypercoagulability pattern was observed regardless of the time of administration of the compound (before or after the ellagic infusion). The silicone clotting times after the infusion of ellagic acid were markedly shortened and remained so for about 60 minutes. The results observed in two control groups treated with saline were similar. The euglobulin lysis times were clearly prolonged after the administration of tranexamic acid, whereas no changes were observed after the administration of saline. These results indicate that tranexamic acid has no anti-factor XII activity.

Animals↗
PubMed2001

Plasma tranexamic acid concentrations during cardiopulmonary bypass.

UNLABELLED: Although tranexamic acid is used to reduce bleeding after cardiac surgery, there is large variation in the recommended dose, and few studies of plasma concentrations of the drug during cardiopulmonary bypass (CPB) have been performed. The plasma tranexamic acid concentration reported to inhibit fibrinolysis in vitro is 10 microg/mL. Twenty-one patients received an initial dose of 10 mg/kg given over 20 min followed by an infusion of 1 mg. kg(-1). h(-1) via a central venous catheter. Two patients were removed from the study secondary to protocol violation. Perioperative plasma tranexamic acid concentrations were measured with high-performance liquid chromatography. Plasma tranexamic acid concentrations (microg/mL; mean +/- SD [95% confidence interval]) were 37.4 +/- 16.9 (45.5, 29.3) after bolus, 27.6 +/- 7.9 (31.4, 23.8) after 5 min on CPB, 31.4 +/- 12.1 (37.2, 25.6) after 30 min on CPB, 29.2 +/- 9.0 (34.6, 23.8) after 60 min on CPB, 25.6 +/- 18.6 (35.1, 16.1) at discontinuation of tranexamic acid infusion, and 17.7 +/- 13.1 (24.1, 11.1) 1 h after discontinuation of tranexamic acid infusion. Four patients with renal insufficiency had increased concentrations of tranexamic acid at discontinuation of the drug. Repeated-measures analysis revealed a significant main effect of abnormal creatinine concentration (P = 0.02) and time (P < 0.001) on plasma tranexamic acid concentration and a significant time x creatinine concentration interaction (P < 0.001). IMPLICATIONS: A 10 mg/kg initial dose of tranexamic acid followed by an infusion of 1 mg.kg(-1).h(-1)produced plasma concentrations throughout the cardiopulmonary bypass period sufficient to inhibit fibrinolysis in vitro. The dosing of tranexamic acid may require adjustment for renal insufficiency.

Adult↗
PubMedDate not supplied

Stability and release of topical tranexamic acid liposome formulations.

Tranexamic acid (TA) has been claimed to have whitening effects. The effects of TA contents (5% and 10%) and charges on the stability and release of TA entrapped in hydrogenated soya phosphatidylcholine/cholesterol/charged lipid [dicetyl phosphate (-) or stearylamine (+)] liposomes at molar ratios of 7:2:1(-) and 7:2:1 (+) were investigated. The TA contents were determined spectrophotometrically at 415 nm, following derivatization with 2,4,6-trinitrobenzosulfonic acid. Stability and leakage of TA from liposomes were characterized at 4 degrees, 30 degrees and 45 degrees C for 90 days. The leakage rates of TA in negative liposomes were lower than those in positive liposomes. The TA in all liposome formulations was relatively stable, as > 90% of total drug remained after up to two months. The release of TA from liposomes was examined using vertical Franz diffusion cells at 37 degrees C for 24 h. The release rates of TA from all liposome formulations were approximately 3 times lower than those from solutions. Charges appeared to affect the physical stability, leakage, and shelf life of TA in liposomes, whereas TA concentrations seemed to affect the release of TA. The 7:2:1 (10% TA,-) liposome was the best formulation, due to its small size, low leakage, high stability, and prolonged and sustained release profile.

Administration, Topical↗
PubMed1976

Diffusion of tranexamic acid to the joint.

Tranexamic acid (Cyklokapron, Kabi, Stockholm) in a dose of 10 mg per kg body weight was given i.v. to 17 patients at various intervals before operation on the knee joint, in order to elucidate the diffusion of the drug to the joint fluid and the synovial membrane. The acid diffused rapidly to both the above tissues, and in the joint fluid it reached the same concentration as in the serum. The biologic half-time in the joint fluid was about 3 hours. In the treatment of joint bleedings in hemophiliacs and in association with intra-articular operations on such patients tranexamic acid is a suitable supplement to conventional substitution therapy.

Adult↗
PubMed1995

The dose-response relationship of tranexamic acid.

BACKGROUND: Prophylactic administration of the antifibrinolytic drug tranexamic acid decreases bleeding and transfusions after cardiac operations. However, the best dose of tranexamic acid for this purpose remains unknown. This study explored the dose-response relationship of tranexamic acid for hemostatic efficacy after cardiac operation. METHODS: In prospective, randomized, double-blinded fashion, 148 patients undergoing cardiac operation with extracorporeal circulation were divided into six groups: a placebo group and five groups receiving tranexamic acid in loading doses before incision (range 2.5 to 40 mg.kg-1) and one-tenth the loading dose hourly for 12 h. The mass of blood collected by chest tubes over 12 h represented blood loss. Allogeneic transfusions within 12 h and within 5 d of surgery were tallied. RESULTS: The six groups presented similar demographics. Patients receiving placebo had increased postoperative D-dimer concentration compared to groups receiving tranexamic acid. Patients receiving at least 10 mg.kg-1 tranexamic acid followed by 1 mg.kg-1.h-1 bled significantly less (365, 344, and 369 g.12 h-1, respectively, for those three groups) compared with patients who received placebo (552 g, P < 0.05). Tranexamic dose did not affect transfusions. Only initial hematocrit affected whether a patient received an allogeneic transfusion within 5 days of operation (odds ratio 2.08 for each 3% absolute decrease in hematocrit). CONCLUSIONS: Prophylactic tranexamic acid, 10 mg.kg-1 followed by 1 mg.kg-1.h-1, decreases bleeding after extracorporeal circulation. Larger doses do not provide additional hemostatic benefit.

Adult↗