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PubMed1977

The effect of fibrinolytic inhibition in the resolution of experimental vitreous hemorrhage.

Complete inhibition of vitreous fibrinolytic activity with 4-amino-methylcyclohexane carbonic acid was associated with significantly delayed resolution of vitreous hemorrhages in rabbits. However, polyacrylamide gel electrophoresis indicated but a slight delay in the removal of the fibrin component of vitreous clots, and most of the residual vitreous opacity comprised intact red blood cells. Fibrin degradation products may act as chemotactic agents, promoting the removal of red blood cells by leukocytes; hence, their absence in treated rabbits might explain in part the delayed red blood cell clearance.

Absorption↗
PubMed1978

Allosteric effects of some antifibrinolytic amino acids on the catalytic activity of human plasmin.

The effects of L-lysine, 6-aminohexanoic acid, and trans-4-aminomethylcy-clohexane-1-carboxylic acid on the catalytic activity of plasmin (EC 3.4.21.7) have been investigated. The kinetics of the plasmin-catlysed hydrolysis of alpha-N-benzoyl-L-arginine ethyl ester in the presence of these compounds have been studied at a number of different concentrations of the three modifiers. They each exert two effects on the reaction, an activation and an inhibition, the concentration dependencies of which are markedly different. They must therefore arise from two different interactions between plasmin and the modifier. The inhibition is competitive, so that it most probably results from direct interaction at the catalytic site. The activation is kinetically non-competitive. The experimental observations seem to be explained best by assuming that L-lysine and certain analogous compounds function as both allosteric modifiers and competitive inhibitors of plasmin.

Allosteric Regulation↗
PubMed1992

Positive co-operative binding at two weak lysine-binding sites governs the Glu-plasminogen conformational change.

The kinetics of a series of Glu-plasminogen ligand-binding processes were investigated at pH 7.8 and 25 degrees C (in 0.1 M-NaCl). The ligands include compounds analogous to C-terminal lysine residues and to normal lysine residues. Changes of the Glu-plasminogen protein fluorescence were measured in a stopped-flow instrument as a function of time after rapid mixing of Glu-plasminogen and ligand at various concentrations. Large positive fluorescence changes (approximately 10%) accompany the ligand-induced conformational changes of Glu-plasminogen resulting from binding at weak lysine-binding sites. Detailed studies of the concentration-dependencies of the equilibrium signals and the rate constants of the process induced by various ligands showed the conformational change to involve two sites in a concerted positive co-operative process with three steps: (i) binding of a ligand at a very weak lysine-binding site that preferentially, but not exclusively, binds C-terminal-type lysine ligands, (ii) the rate-determining actual-conformational-change step and (iii) binding of one more lysine ligand at a second weak lysine-binding site that then binds the ligand more tightly. Further, totally independent initial small negative fluorescence changes (approximately 2-4%) corresponding to binding at the strong lysine-binding site of kringle 1 [Sottrup-Jensen, Claeys, Zajdel, Petersen & Magnusson (1978) Prog. Chem. Fibrinolysis Thrombolysis 3, 191-209] were observed for the C-terminal-type ligands. The finding that the conformational change in Glu-plasminogen involves two weak lysine-binding sites indicates that the effect cannot be assigned to any single kringle and that the problem of whether kringle 4 or kringle 5 is responsible for the process resolves itself. Probably kringle 4 and 5 are both participating. The involvement of two lysine binding-sites further makes the high specificity of Glu-plasminogen effectors more conceivable.

Aminocaproic Acid↗
PubMed1989

Healing of gastric ulcer in the elderly: a double-blind study of cetraxate versus ranitidine.

Forty-nine Chinese patients, ages 65 years or over, with endoscopically and pathologically diagnosed benign gastric ulcer, completed a randomized double-blind double dummy trial in treatment with either cetraxate 200 mg four times daily or ranitidine 150 mg two times daily for 12 weeks or less if the gastric ulcer had completely healed. All patients tolerated the procedure well. At the end of the 4th, 8th, and 12th weeks ulcer healing was complete in 2 (8%), 11 (42%), and 17 (65%), respectively, of the cetraxate group (26 patients); and in 8 (35%), 18 (78%), and 22 (96%), respectively, of the ranitidine group (23 patients). All the differences in the healing rates were statistically significant. Pain relief was significantly earlier with ranitidine. Incidences of side effects were similar and not serious in the two groups. The results suggest that at the doses prescribed to the elderly, ranitidine is significantly more effective than cetraxate in gastric ulcer healing and pain relief.

Aged↗
PubMed1983

Effects of fibrinolytic treatment on rabbit Masugi nephritis.

We investigated the effects of administration of urokinase (UK) and trans-4-aminomethylcyclohexane carboxylic acid (t-AMCHA) on the development of experimental rabbit Masugi nephritis. Treatment with 1000 U/kg of UK, 5000 U/kg of UK and 100 mg/kg of t-AMCHA twice a day intravenously was initiated on the 7th and continued for 7 consecutive days. Concomitantly with the nephrotoxin injection, 5000 U/kg of UK was also given twice a day intravenously for 14 days. The administration of 5000 U/kg of UK twice a day for 7 days and 14 days suppressed the increases in BUN values and the decreases in urinary fibrinolytic activity. Fibrin-fibrinogen degradation products (FDP) were detected more frequently in the urine of rabbits given UK than in the control. Immunofluorescence microscopy showed a decrease in intra- and extra-glomerular fibrin deposition, and a decrease in fibrin or fibrinoid deposits in Bowman's space by 5000 U/kg of UK was demonstrated electron microscopically. Light microscopy revealed that the accumulation of fibrin in glomeruli, crescent formation, and progressive glomerular disorganization by 5000 U/kg of UK were prevented. On the other hand, treatment with t-AMCHA enhanced the increase in BUN values and there was a decrease in urinary fibrinolytic activity. Dense fibrin deposits in the glomeruli, were observed immunopathologically by treatment with t-AMCHA and histopathologic changes were found to be even more severe.

Animals↗
PubMed1982

Effect of EACA, PAMBA, AMCA and AMBOCA on fibrinolysis induced by streptokinase, urokinase and tissue activator.

A study is presented in which the inhibiting effects of eACA, PAMBA, AMCA and AMBOCA on fibrinolysis induced by three activators have been compared by a clot lysis method. The order of inhibitory potency was AMBOCA greater than AMCA greater than PAMBA greater than EACA. The activity ratios obtained were found to be influenced by the level of inhibition. At low levels of inhibition the differences between the inhibitory activities are usually more pronounced than at high levels. The degree of inhibition is dependent on the fibrinolytic activator used. The order of sensitivity to the inhibitors was, within the analytical conditions used, found to be: tissue activator greater than streptokinase greater than urokinase. The results are discussed in comparison to the different activity ratios reported by others.

4-Aminobenzoic Acid↗
PubMed2003

Suppression of argatroban-induced endogenous thrombolysis by PKSI-527, and antibodies to TPA and UPA, evaluated in a rat arterial thrombolysis model.

We have previously confirmed, using a rat mesenteric arteriole thrombolysis model, that thrombin inhibition induces endogenous thrombolysis in vivo. In addition, we have shown that thrombin-activatable fibrinolysis inhibitor (TAFI) plays a role in the down regulation of endogenous thrombolysis. However, the mechanism of endogenous thrombolysis or spontaneous plasmin generation in vivo remains unclear. It has been shown in an in vitro system that plasma kallikrein activates pro-urokinase (pro uPA) and/or plasminogen, resulting in plasmin generation. These findings suggest that spontaneous fibrinolysis might be mediated by tPA and plasma kallikrein-dependent uPA. The aim of the present study was to examine whether these mechanisms play a dominant role in endogenous thrombolysis in vivo, using our rat mesenteric arterial thrombolysis model. Argatroban infusion enhanced endogenous thrombolysis. PKSI-527, anti uPA and anti tPA IgGs suppressed argatroban-induced thrombolysis. Also, the antibody IgG preparations suppressed endogenous thrombolysis in the absence of argatroban. In the presence of PKSI-527, anti tPA IgG was more effective than anti uPA IgG in suppressing argatroban-induced thrombolysis. The results suggested that both tPA and plasma kallikrein-mediated uPA activation and tPA release contribute to endogenous fibrinolytic or thrombolytic mechanisms.

Animals↗
PubMedDate not supplied

[Willebrand disease].

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Aminocaproic Acid↗
PubMed1986

Antifibrinolytic therapy in the treatment of aneurysmal subarachnoid hemorrhage.

At the present time, there remains considerable uncertainty regarding the safety and efficacy of antifibrinolytic therapy in the treatment of aneurysmal SAH. Furthermore, there is little to guide us on precisely how to employ the agents. Whether to continue to use antifibrinolytic therapy after considering the results of the 1984 Cooperative Aneurysm Study trial and the Glasgow-Rotterdam-Amsterdam-London trial remains very much a philosophical decision. However, rebleeding is instantly and permanently devastating and 70% fatal, while ischemic deficits from vasospasm have a gradual onset and are potentially reversible. Accordingly, our policy is to continue to use antifibrinolytic therapy in those patients in whom it is desired to delay surgery. Our feeling is that, while there is no demonstrated advantage in acute mortality in either of the previously mentioned series, hypertensive, hypervolemic therapy or calcium channel blocking agents might ameliorate the ischemic consequences of therapy. Accordingly, it is in the context of combined therapy that the reduction in rebleeding will significantly influence patient outcome.

4-Aminobenzoic Acid↗
PubMed1981

Selective inhibition of collagen breakdown by proteinase inhibitors in granulation tissue in rats.

A rapid breakdown of collagen was found in granulation tissue induced by carrageenin in rats; the half-life of collagen in both growing and resorbing tissues was about 3.5 days, whereas that in non-resorbing tissue was about 7 days. On the other hand, the half-life of noncollagen protein in the growing, resorbing and non-resorbing tissues was about 2-3 days. epsilon-Amino-n-caproic acid n-hexyl ester, an inhibitor of plasmin and trypsin, selectively inhibited collagen breakdown in vivo without affecting the degradation of noncollagen protein or the syntheses of collagen and noncollagen protein in granulation tissues. A similar selective inhibition of collagen breakdown was also found upon treatment with soybean trypsin inhibitor. Collagenase activity was assayed directly in the insoluble 6,000 X g pellet of granulation tissue homogenates. epsilon-Amino-n-caproic acid n-hexyl ester and soybean trypsin inhibitor markedly inhibited the collagen breakdown in granulation tissue pellets in vitro. The results are consistent with those from in vivo experiments and suggest that both the inhibitors indirectly inhibit the collagen breakdown in granulation tissue through the inhibition of a latent collagenase-activating proteinase(s), because none of the inhibitors directly inhibit collagenase. It may be argued, therefore, that a proteinase(s) which activates a latent collagenase plays an important role in the rapid breakdown of collagen in granulation tissues.

Aminocaproates↗
PubMed1998

Aprotinin versus lysine analogues: the debate continues.

The decision to use any pharmacologic intervention inevitably rests on balancing the efficacy and safety of the intervention. The advent of the acquired immunodeficiency syndrome epidemic greatly increased awareness of transfusion-related illnesses and focused attention on methods to prevent the need for blood and blood products. This has led, especially in the last decade, to increased use of drugs to help reduce perioperative bleeding. This chapter focuses on the lysine analogues and aprotinin as the serine protease inhibitor currently available in clinical practice. Both groups of compounds have recently shown promise in reducing surgical bleeding. However, the reader will notice that none of these agents are new; they have all been available for more than 30 years. What is new is their use in preventing bleeding. We therefore have considerable knowledge regarding the safety of these compounds. The first part of this review will compare the actions of these two types of agents on the processes related to thrombosis, hemostasis, and fibrinolysis. This is followed by a comparison of the efficacy of each intervention and any dose-response relationship. This section highlights the reported reduction in postoperative bleeding with both classes of agent. There is, however, no obvious or consistent reduction in the transfusion of blood and blood products in patients given lysine analogues. In contrast, there is a consistent reduction in the need for blood transfusions in patients given aprotinin therapy. The next major section will discuss the evidence to suggest that these drugs may, because of their known effects on the processes related to inflammation, hemostasis, and cellular repair, contribute to an improvement or worsening of outcome after cardiac operations. In particular, this section focuses on the antiinflammatory actions and modifications in vascular tone associated with aprotinin therapy. These effects may be related to improved outcome in patients by reducing the incidence of permanent neurologic deficit or stroke after heart operations, as well as inhibiting pulmonary vascular hyperreactivity and hypertension in susceptible individuals. Finally, this brief review discusses the safety issues that have been raised in regard to each of these classes of agents, specifically problems associated with abnormal renal function, hypersensitivity reactions, and thrombotic complications.

Aminocaproic Acid↗