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PubMed1986

The autodigestion of human plasmin follows a bimolecular mode of reaction subject to product inhibition.

Plasmin is a labile enzyme destroyed by a process termed autodigestion. Studied by a kinetic assay on the substrate Tos-Gly-Pro-Lys-pNA this process is shown to follow a bimolecular mode of reaction, which is retarded by plasmin degradation products. Plasmin is protected by fibrinogen, by epsilon-aminocaproic acid (6-aminohexanoic acid), by increasing ionic strength, and by glycerol. CNBr fragments of fibrinogen did not protect. Lack of substrate protection of plasmin may give rise to errors in a two-stage plasminogen activator assay, while the presence of substrate in a one-stage method prevents degradation of the generated plasmin.

Aminocaproic Acid↗
PubMed1983

DDAVP: review of indications for its use in the treatment of factor VIII deficiency and report of a case.

Classic hemophilia or factor VIII deficiency is a recessive, sex-linked bleeding diathesis. The primary clinical problem is hemorrhage, which can be severe and often life threatening, even in the presence of only minor trauma. In the past this inadequate hemostasis has been treated with transfusions of cryoprecipitate, fresh frozen plasma, or commercially prepared factor VIII concentrate. Unfortunately, such treatment carries with it a number of risks, including the development of hepatitis B or hemolytic anemia and the formation of anti-factor VIII antibodies. Because of hemorrhage severity and the risks of conventional treatment, elective surgery in general and oral surgery in particular have often been neglected in patients with hemophilia. This article reviews a drug, 1-desamino-8-d-arginine (DDAVP), heretofore not discussed in the dental literature, and reports on its use in conjunction with epsilon-aminocaproic acid (EACA), a synthetic antifibrinolytic agent, in the surgical dental treatment of a patient with hemophilia A. The results suggest that certain dental surgical procedures can be performed in the presence of subclinical and mild hemophilia without conventional factor VIII replacement therapy with its associated costs and risks.

Adult↗
PubMed1997

Enzyme-controlling medicines: introduction.

A short history of the research work of S. Okamoto and co-workers, for the previous 50 years, is briefly described. In the 1950s, when the physiologic role of fibrinolysis had not been established, they began to seek for compounds that inhibit the action of plasmin. They examined approximately 200 lysine derivatives and discovered epsilon aminocaproic acid (EACA) and tranexamic acid (t-AMCHA). In the 1970s, we selected thrombin as the target enzyme to be controlled; structure-activity relationship studies, taking arginine as the skeleton structure, led to the discovery of the selective thrombin inhibitor No. 205 (4-ethyl-1-[N2-(5-dimethylamino-1-naphthalenesulfonyl)-L-arginyl]- 1-piperidine), and further attempts to minimize the toxicity finally led to No. 805 (argatroban, MD-805, (2R,4R)-4-methyl-1-(N2-[(3-methyl-1,2,3,4-tetrahydro-8-quinolinyl)-sulfo nyl]-L-arginyl)-2-piperidine carboxylic acid). Argatroban, without any cofactor, inhibits thrombin competitively. The high selectivity of the action of argatroban is promising for treating thrombosis in clinical practice. More recently, taking advantage of our knowledge obtained through previous studies, active center-directed plasmin inhibitors and a selective inhibitor of kallikrein have been found.

Aminocaproic Acid↗
PubMed1979

Glanzmann's thrombasthenia. Report of two oral surgical cases using a new microfibrillar collagen preparation and EACA for hemostasis.

Glanzmann's thromboasthenia is a rare congenital platelet disorder characterized by a prolonged bleeding time, a qualitative platelet defect, and severe hemorrhagic episodes. Patients with this disorder have been managed by administration of blood and blood components (most recently, platelet-rich plasma and platelet concentrates) to control hemorrhage resulting from trauma or surgical procedures. The two case reports presented here illustrate the use of a local hemostatic agent (microfibrillar bovine collagen, Avitene) and a systemic fibrinolytic inhibitor (epsilon aminocaproic acid, Amicar) to control postoperative hemorrhage secondary to elective extraction of teeth. The clinical results demonstrate excellent postoperative hemostasis and support recent in vitro observation of platelet adherence to the collagen preparation. This provides an alternate therapeutic modality in the management of patients with Glanzmann's disease and possibly other disorders of platelet function.

Abscess↗
PubMed1989

Highly potent and small neuropeptide Y agonist obtained by linking NPY 1-4 via spacer to alpha-helical NPY 25-36.

Analogues of neuropeptide Y (NPY) containing small N- and C-terminal segments linked via flexible spacer arms were found to exhibit receptor binding affinity constants almost as high as NPY as well as post- and presynaptic NPY-agonistic activities. One of the most active analogues contains N-terminal NPY segment 1-4 linked via epsilon-aminocaproic acid (Aca) to the C-terminal partially alpha-helical peptide amide segment 25-36. NPY 1-4-Aca-25-36 is the first highly potent NPY agonist, which is of considerably reduced size in comparison to the native hormone. The analogues are accessible by solid-phase synthesis using Fmoc strategy.

Aminocaproic Acid↗
PubMed1989

Intraoperative coagulation changes in children undergoing liver transplantation.

Intraoperative changes in blood coagulation were observed in eight children undergoing liver transplantation using a simplified coagulation profile (prothrombin time [PT], activated partial thromboplastin time [aPTT], and platelet count) and thrombelastography. Preoperatively, PT and aPTT were moderately prolonged (1.5 times control), and platelet count was greater than 100,000/mm3 in all patients but one (91,000/mm3). During the preanhepatic and anhepatic stages, PT, aPTT, reaction time, and coagulation time improved toward normal values, but platelet count and maximum amplitude did not change. Significant changes in coagulation occurred on reperfusion of the grafted liver: PT, aPTT, reaction time, and coagulation time were prolonged, and platelet count, maximum amplitude, and clot formation rate decreased. A heparin effect, which did not require treatment, was seen on reperfusion in four patients. Fibrinolysis occurred during the operation in five patients and was treated with Epsilon-aminocaproic acid (EACA) in one. Blood coagulation improved slowly, and values were close to baseline 90 min after reperfusion. In general, the coagulation changes seen in these children are similar to those in adults but less severe, possibly because of the preponderance of cholestatic disease in children compared with the more common hepatocellular disease in adults.

Aminocaproic Acid↗
PubMed1998

[Common variable immunodeficiency associated with autoimmune thrombocytopenia: anesthetic management].

A 44-year-old man diagnosed of common variable immunodeficiency associated with thrombopenia due to autoimmunity required anesthesia for anal fissure repair and hemorrhoidectomy. Hemostatic complications developed after surgery, with extreme thrombopenia (1,000 platelets/pl) and analytical changes that necessitated administration of six units of platelets from apheresis, as well as immunoglobulins, antifibrinolytic agents (e-aminocaproic acid) and granulocytic colony stimulating factors. Anesthesia for such patients is reviewed, with emphasis on careful management of the airways, preparation of sufficient material for surgery (rapid transfusion equipment, large caliber intravenous catheters, sterile material) and orientation of anesthetic technique toward general anesthesia through a laryngeal mask.

Adjuvants, Anesthesia↗
PubMed1989

[Antiplasmin drugs and factor XIII concentrates in the treatment of a patient with acute promyelocytic leukemia (M3)].

A female patient what M3 was seen to incur marked hemorrhagic diathesis during therapy. Heparin infusion was performed to inhibit disseminated intravascular coagulation (DIC). However, oozing from the puncture site of the r-subclavian vein was observed. Her data on coagulation were as follows: AT-3 greater than 100%, fibrinogen 69.0 mg, XIII less than 40%, FPA 2.9 ng/ml and FDP-D dimer 256 ng/ml. The alpha-2-plasmin inhibitor (alpha 2-PI) was 44% and FDP 160 microgram/ml. These results suggested DIC with activated fibrinolysis. Thus, epsilon aminocaproic acid in conjunction with heparin, fibrinogen, and concentrated XIII was administered. The abnormal bleeding improved with an increase of alpha 2-PI and XIII. This clinical response indicated that an activated fibrinolysis and a decreased XIII might have been responsible for provoking the bleeding of the patient.

Adult↗
PubMed1993

The platelet-refractory bone marrow transplant patient: prophylaxis and treatment of bleeding.

Refractoriness to platelet transfusions remains a significant problem for oncology patients, occurring in 30% to 70% of multiply transfused recipients with bone marrow failure. Nonimmune causes are often present and include disseminated intravascular coagulation, concurrent use of amphotericin B, infection, presence of palpable spleen, use of antibacterial antibiotics, bleeding, veno-occlusive disease, and fever. Immune causes are also commonly responsible for refractoriness, with HLA alloimmunization dominating the list of immune factors. HLA antibodies can be identified in 25% to 30% of transfused leukemia patients and can be present in as many as 80% of aplastic anemia patients. Developing a consistent approach to managing these refractory patients is essential to preventing and treating bleeding manifestations. An HLA type should be obtained for all patients anticipated to have chronic transfusion requirements. Screening for lymphocytotoxic antibodies can confirm suspected HLA alloimmunization. Histocompatible platelets (cross-match compatible and HLA matched) should be provided for all patients with HLA antibodies. A number of other therapeutic modalities have been used in an effort to manage the alloimmunized patient; most of these methods have had little or no proven benefit. When bleeding develops in the alloimmunized patient, there are few therapeutic choices. If histocompatible platelets are unavailable or unsuccessful, massive platelet transfusions of pooled platelet concentrates are commonly used, although this practice is of no proven benefit. While antifibrinolytic agents have been available for over 30 years, they are only recently being applied to control bleeding in chronic thrombocytopenia. We have successfully managed bleeding episodes in thrombocytopenic bone marrow transplant recipients with the use of epsilon aminocaproic acid. A number of these patients were platelet refractory with demonstrable platelet antibodies. Platelet refractoriness continues to plague multiply transfused oncology patients. While preventative measures may ultimately benefit some patients, this problem will continue to manifest itself. A consistent approach to transfusion support needs to be implemented to best manage this challenging patient population.

Aminocaproic Acid↗
PubMed1998

Identification of two laminin-binding fimbriae, the type 1 fimbria of Salmonella enterica serovar typhimurium and the G fimbria of Escherichia coli, as plasminogen receptors.

Escherichia coli strains carrying recombinant plasmids encoding either the type 1 fimbria of Salmonella enterica serovar Typhimurium or the G fimbria of E. coli exhibited binding of human 125I-Glu-plasminogen and enhanced the tissue-type plasminogen activator-catalyzed conversion of plasminogen to plasmin. Purified type 1 or G fimbriae similarly bound plasminogen and enhanced its activation. The binding of plasminogen did not involve the characteristic carbohydrate-binding property of the fimbriae but was inhibited at low concentrations by the lysine analog epsilon-aminocaproic acid. Because these fimbrial types bind to laminin of basement membranes (M. Kukkonen et al., Mol. Microbiol. 7:229-237, 1993; S. Saarela et al., Infect. Immun. 64:2857-2860, 1996), the results demonstrate a structural unity in the creation and targeting of bacterium-bound proteolytic plasmin activity to basement membranes.

Aminocaproic Acid↗
PubMed1989

Binding of plasminogen to Escherichia coli adhesion proteins.

Immobilization of plasminogen via its lysine-binding sites is regarded as a prerequisite for its activation and function in fibrinolysis and pericellular proteolysis. In the present study, the interaction of plasminogen with fimbriae found on Escherichia coli strains causing invasive human infections was studied. Plasminogen displayed concentration-dependent and saturable binding to immobilized type 1 fimbriae and, several fold lower binding to P and S fimbriae. The binding to fimbriae was effectively inhibited by epsilon-aminocaproic acid indicating that it was mediated by the lysine-binding sites of plasminogen. Binding studies with mutated fimbriae and inhibition tests indicated that the interaction was not dependent on the lectin subunit of the fimbriae. These results indicate the existence of a novel type of host-microbe interaction which may be important in the invasion by bacteria of host tissues.

Adhesins, Escherichia coli↗
PubMed1978

A practical proposal for arginine-vasopressin radioimmunoassay.

This work proposes the use of (a) a commercially available homologous system AVP antibody-AVP (Arginine Vasopressin) standard and (b) new acquisitions for the improvement of sensitivity for AVP radioimmunoassay by separate or simultaneous use of two-phase sequential incubation and epsilon-aminocaproic acid (EACA). The antiserum used in the system described is very specific since none even cross-reacted with lysine vasopressin (LVP) and has an apparent affinity constant (K) of 0.909 +/- 0.047 X 10(12) l/mol. This is sufficiently high to detect 0.5 +/- 0.2 pg/tube, which is theoretically expected of biological AVP. The total assay time is less than 48 h.

Aminocaproic Acid↗
PubMed1980

Afibrinogenemia following snake bite (Crotalus durissus terrificus).

Following the bite of Crotalus durissus terrificus, an 11-year-old boy developed afibrinogenemia and high output acute renal failure. His platelet count remained within normal limits. He was treated with epsilon aminocaproic acid and whole fresh blood transfusion, with full recovery from afibrinogenemia 40 hours after the beginning of these measures and 75 hours after the snake bite. No hemorrhagic disturbances were present. The acute renal failure was treated conservatively, and the patient recovered 12 days after the snake bite and discharged from hospital with no sequelae.

Acute Kidney Injury↗
PubMed1980

A comparison of the effects of intravenous serotonin and dextran on the levels of factor XII, prekallikrein and plasminogen in rat plasma.

It was previously observed that serotonin injected intravenously into the rat caused significant reductions in the prekallikrein activator (PKA) and the benzoyl arginine ethyl ester (BAEe)-esterase activities induced in rat plasma by acetone/kaolin activation. In the present work it was demonstrated that serotonin was unable to exert these effects in vitro, in plasma or in whole blood. The assay of PKA and Baee-esterase activities after gel filtration on Sephadex G-100 of acetone-activated plasma from rats treated with serotonin 0.10 mg/kg revealed reduced fragmentation of factor XII, and reduced levels of kallikrein and of an additional BAEe-esterase. Serotonin also lowered the plasminogen level. The serotonin-induced reductions of PKA and BAEe-esterase were inhibited by pretreatment of the rats with epsilon-aminocaproic acid. Evidence was provided that serotonin did not lower the plasma level of factor XII of the coagulation system, but the level of a factor of significance for the activation of factor XII. All the above-mentioned serotonin effects were fundamentally similar to the corresponding effects caused by dextran. It is concluded that the effects of dextran on the plasma parameters mentioned are mediated by the release of endogenous serotonin.

Aminocaproic Acid↗
PubMed1979

Cerebral thrombosis associated with Amicar therapy.

Amicar (epsilon-aminocaproic acid) has been used in patients with subarachnoid hemorrhage to promote clotting. However, cerebral thrombosis has been reported in various vascular compartments following its use. The authors describe 2 patients who had cerebral angiography after Amicar therapy and demonstrated thrombosis unrelated to vascular spasm or technical complications of angiography. Careful screening is needed in patients treated with Amicar to determine if an increased risk of thrombosis exists.

Adult↗
PubMed1991

Prevention of in vitro fibrinogenolysis during laboratory monitoring of thrombolytic therapy with streptokinase or APSAC.

In the present study, we systematically investigated aprotinin, epsilon-aminocaproic acid (EACA) and tranexamic acid as inhibitors of fibrinogen breakdown and of the generation of fibrinogen degradation products (FgDP). The experimental setting very closely imitated the conditions in practice when collecting blood from patients receiving thrombolytic therapy with streptokinase or APSAC. The minimal concentration of aprotinin required to completely inhibit fibrinogen breakdown and FgDP generation was 200 KIU/ml blood. This was sufficient even at the highest concentrations of streptokinase and APSAC expected to occur in patients (300 U/ml and 46 nM, respectively). However, 200 KIU/ml aprotinin heavily interfered in the determinations of plasminogen and alpha 2-antiplasmin. Relatively low concentrations of EACA (200 mM) and tranexamic acid (35 mM) were sufficient to prevent FgDP generation, but they interfered in the Clauss assay of fibrinogen. A non-interfering concentration of EACA (7 mM) allowed the inhibition of lower concentrations of APSAC (20 nM) and streptokinase. We conclude that at least 200 KIU aprotinin per ml blood is necessary to effectively inhibit in vitro fibrinogenolysis under circumstances likely to be met in clinical practice during thrombolytic therapy.

Aminocaproic Acid↗
PubMedDate not supplied

[Role of the K4 and K5 plasmin heavy chain kringles in the fibrin clot structure destruction].

A comparative analysis of the rates of polymeric fibrin structure destruction by plasmin (Pm) and its proteolytic derivatives such as Val354-plasmin (c-Pm), Val442-plasmin (m-Pm) and Lys530-plasmin (mu-Pm) has been undertaken. It was shown, that Pm, c-Pm, m-Pm and mu-Pm at equal proteolytic activity, have dissolved fibrin clots with relative rates 40.3:38.0:4.6:1.0 correspondingly. The Pm, m-Pm and mu-Pm relative rates were changed by epsilon-aminocaproic acid to 4.6:1.5:1.0 correspondingly. In this case fibrin clot destruction time was increased for Pm and m-Pm and was not changed for mu-Pm. The rates of fibrinogen hydrolysis were nearly equal for these forms of enzyme. It was suggested, that the specific interactions between plasmin K4 and K5 kringles and solid phase fibrin substrate determine the polymer fibrin structure destruction rate.

Aminocaproic Acid↗
PubMed1996

Interaction of a recombinant form of apolipoprotein[a] with human fibroblasts and with the human hepatoma cell line HepG2.

We have studied the binding, uptake, and degradation of a recombinant form of apolipoprotein[a] (r-apo[a]) using a cultured cell model. In HepG2 cells and in human fibroblasts, r-apo[a] complexed with low density lipoprotein(LDL) is bound and internalized via high affinity (Kd = 10 nM) receptors; in both cell types, low affinity (Kd = 200-300 nM) sites also mediate free apo[a] uptake. Using competition studies, we found that the high affinity binding component corresponds to the LDL receptor. Involvement of the LDL receptor in r-apo[a] uptake by fibroblasts was confirmed using fibroblasts derived from an individual homozygous for familial hypercholesterolemia; in contrast to normal fibroblasts, these cells lacked the high affinity r-apo[a] binding component. Cell association of 125I-labeled r-apo[a] was increased and decreased concomitantly with the up- and down-regulation of the LDL receptor in response to a number of compounds. The addition of alpha 2-macroglobulin as well as treatment with heparinase, chondroitinase ABC, and sodium chlorate did not decrease total specific binding of r-apo[a], suggesting that neither the low density lipoprotein receptor-related protein nor cell surface proteoglycans are involved in r-apo[a] clearance. The low affinity binding component present in both fibroblasts and HepG2 cells likely corresponds to the plasminogen receptor, as binding of r-apo[a] to these sites was specifically decreased by the addition of plasminogen or the lysine analogue epsilon-aminocaproic acid, but not by the addition of tissue-type plasminogen activator. Heparin abolished uptake of r-apo[a] by the LDL receptor component only; this indicates that apo[a] must be associated with LDL to be cleared by this receptor. In contrast, free apo[a] can be effectively cleared by the plasminogen receptor which may represent a significant route of clearance for free apo[a] in vivo.

Aminocaproic Acid↗