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PubMed1983

The role of plasminogen activator in ovulation.

The role of plasminogen activator in ovulation was investigated using the inhibitor, trans-aminomethylcyclohexane carboxylic acid (t-AMCHA). In the regular cycle rat, the plasminogen activator activity of the follicles increased from the diestrus to the estrus phase. In the latter phase, a proteolytic enzyme which was not inhibited by t-AMCHA appeared. After ovulation, the plasminogen activator activity decreased. When ovulation was induced in immature rats by pregnant mare serum gonadotrophin and human chorionic gonadotrophin, remarkable fibrinolytic activity appeared in the ovaries immediately before ovulation. When t-AMCHA was given in the ovulation-induced rats, the fibrinolytic activity of the ovaries was suppressed, the number of ovulated ova decreased and the timing of ovulation was delayed. When t-AMCHA solution was given to rats in the proestrus phase, ovulation was almost completely suppressed, but aprotinin solution exerted no effect on ovulation. These results suggest that plasminogen activator is a key enzyme in ovulation, and that the chain reaction from plasminogen activator to proteolytic enzyme (including collagenase) is of greater importance than that of plasminogen activator to plasmin.

Animals↗
PubMed1984

Effect of 2,4-diamino-6-(2,5-dichlorophenyl)-s-triazine maleate (MN-1695) on gastric ulcers and gastric secretion in experimental animals.

The effect of 2,4-diamino-6-(2,5-dichlorophenyl)-s-triazine maleate (MN-1695) on various experimental gastric ulcers and gastric secretion in experimental animals was compared with that of cimetidine and cetraxate. MN-1695 significantly inhibited the formation of Shay, stress-induced, indomethacin-induced, and histamine-induced ulcers and significantly accelerated the healing of acetic acid-induced gastric ulcers. MN-1695 was much more effective in suppressing stress- and acetic acid-induced ulcers than indomethacin-induced, histamine-induced or Shay ulcers. Cimetidine was effective in preventing stress- and acetic acid-induced ulcers but had no significant effect on Shay, indomethacin-induced and histamine-induced ulcers. Cetraxate was effective in preventing only stress-induced ulcers and had almost no effect on other experimental ulcers. MN-1695 inhibited secretion of gastric juice, acid and pepsin in Shay rats, but had no influence on basal and secretagogue-stimulated acid secretion in the perfused stomach of urethanized rats. These findings suggest that MN-1695 is a new type of anti-ulcer agent.

Acetates↗
PubMed2004

Immunohistochemical localization of aspartoacylase in the rat central nervous system.

Aspartoacylase (ASPA; EC 3.5.1.15) catalyzes deacetylation of N-acetylaspartate (NAA) to generate free acetate in the central nervous system (CNS). Mutations in the gene coding ASPA cause Canavan disease (CD), an autosomal recessive neurodegenerative disease that results in death before 10 years of age. The pathogenesis of CD remains unclear. Our working hypothesis is that deficiency in the supply of the NAA-derived acetate leads to inadequate lipid/myelin synthesis during development, resulting in CD. To explore the localization of ASPA in the CNS, we used double-label immunohistochemistry for ASPA and several cell-specific markers. A polyclonal antibody was generated in rabbit against mouse recombinant ASPA, which reacted with a single band (approximately 37 kD) on Western blots of rat brain homogenate. ASPA colocalized throughout the brain with CC1, a marker for oligodendrocytes, with 92-98% of CC1-positive cells also reactive with the ASPA antibody. Many cells were labeled with ASPA antibodies in white matter, including cells in the corpus callosum and cerebellar white matter. Relatively fewer cells were labeled in gray matter, including cerebral cortex. No astrocytes were labeled for ASPA. Neurons were unstained in the forebrain, although small numbers of large reticular and motor neurons were faintly to moderately stained in the brainstem and spinal cord. Many ascending and descending neuronal fibers were moderately stained for ASPA in the medulla and spinal cord. Microglial-like cells showed faint to moderate staining with the ASPA antibodies throughout the brain by the avidin/biotin-peroxidase detection method, and colocalization studies with labeled lectins confirmed their identity as microglia. The predominant immunoreactivity in oligodendrocytes is consistent with the proposed role of ASPA in myelination, supporting the case for acetate supplementation as an immediate and inexpensive therapy for infants diagnosed with CD.

Adenomatous Polyposis Coli Protein↗
PubMed1997

Specificity of ligand-induced conformational change of lipoprotein(a).

The conformation of Lp(a) was probed with a set of omega-aminocarboxylic acids and other analogs of 6-aminohexanoic acid (6-AHA). Using the viscosity-corrected sedimentation coefficient, six additional ligands were shown to induce a major conformational change in Lp(a), from a compact form to an extended form. These were trans-4-(aminomethyl)cyclohexanecarboxylic acid (t-AMCHA), proline, 4-aminobutyric acid, 8-aminooctanoic acid, Nalpha-acetyllysine, and glycine. Lysine, Nepsilon-acetyllysine, glutamic acid, and adipic acid were determined not to cause a conformational change. Urea and guanidine hydrochloride were ineffective at inducing this conformational change at concentrations at which the above ligands did unfold Lp(a). The conformational change was inhibited by 100 mM NaCl and to a lesser extent by 20 mM sodium glutamate. Despite the fact that these two salts have nearly the same ionic strengths, the greater inhibition of the unfolding by NaCl is consistent with a proposed stabilization of interkringle interactions by chloride ions. In 100 mM NaCl, which most closely resembles physiological conditions, only proline, 4-aminobutyric acid, 6-AHA, and t-AMCHA were effective ligands. By analyzing the dimensions of the conformation altering ligands, we propose that a critical variable in determining the effectiveness of a ligand in disrupting Lp(a) is the distance between the carboxyl and amine functions of the ligand. The optimal distance is approximately 6 A, which agrees with the observed 6.6-6.8 A separation of the cationic and anionic centers of known plasminogen and apo(a) lysine binding sites. These studies have implications for the mechanism of Lp(a) particle assembly.

Aminocaproic Acid↗
PubMed1976

Pulmonary damage following pulmonary microembolism in the dog. Effect of various types of treatment.

In the present study the pathogenesis of the pulmonary damage following infusion of thrombin in combination with a fibrinolysis inhibitor, AMCA, in the dog was elucidated. An important mechanism in the development of the pulmonary damage following infusion of thrombin and AMCA seems to be an increased vascular permeability in the pulmonary microvasculature leading to pulmonary oedema. The question whether this pulmonary damage can be prevented by antihistamine (mepyramine maleate), antiserotonins (methysergide, reserpine) antiprostaglandins (acetylsalicylic acid, indomethacin, polyphloretin phosphate), 'anti-inflammatory agents' (methylprednisolone, calcium) or an anti-adrenergic agent (phenoxybenzamine) was investigated. None of these agents did prevent the lung damage following thrombin and AMCA. In order to study the possible role of bronchoconstriction, the complement system and the kinin system for this damage dogs were also artificially ventilated with an increased end-expiratory pressure, decomplemented with cobra venom factor or treated with Trasylol respectively. Neither were these treatments effective in preventing the pulmonary damage. The findings of the present study suggest that the permeability increasing substance involved in the pathogenesis of the pulmonary damage following thrombin and AMCA is not histamine, serotonin, prostaglandins or bradykinin. Therefore another, still unknown factor, may be of greater importance for this damage.

Animals↗
PubMed1998

Aprotinin versus epsilon-aminocaproic acid for aortic surgery using deep hypothermic circulatory arrest.

OBJECTIVE: To compare the relative efficacy of aprotinin and epsilon-aminocaproic acid (EACA) in decreasing blood loss and transfusion requirements after aortic surgery involving deep hypothermic circulatory arrest (DHCA). DESIGN: A retrospective chart review. SETTING: A university medical center. PARTICIPANTS: Forty-nine patients who had undergone thoracic aortic surgery with the use of circulatory arrest. INTERVENTIONS: Charts were examined for variables believed to influence postoperative blood loss, including the use of medications, and for the amount of postoperative chest tube drainage and perioperative transfusion. MEASUREMENTS AND MAIN RESULTS: Median chest tube output (CTO) at 6 and 12 hours postoperatively was nearly identical in patients treated with aprotinin or EACA (660 and 1,015 v 700 and 950 mL for aprotinin and EACA at 6 and 12 hours, respectively), as were total perioperative blood transfusions. Complications were not significantly different between groups with the exception of a trend toward increased incidence of renal failure in the group receiving EACA. CONCLUSION: Aprotinin and EACA appear to be equally efficacious in reducing perioperative blood loss and transfusion requirements in patients undergoing aortic surgery involving DHCA. Questions of safety remain about the use of EACA in this setting that could not be addressed by this small retrospective study. A prospective, placebo-controlled study is warranted to confirm the absolute efficacy of these agents and to better define safety issues.

Adult↗
PubMed1984

Modulators of plasma fibronectin response during sepsis.

Plasma fibronectin (PFN) depletion has been associated with poor outcome in patients with sepsis or those who have experienced trauma; restoration of normal levels appears beneficial. PFN synthesis is increased after cecal ligation even in malnourished animals with sepsis, implying that stimulation of endogenous PFN synthesis is possible. One hundred rats received either a single therapeutic agent (gelatin, heparin, indomethacin, urokinase, captopril, or endotoxin) or the combination of a cecal ligation and a single agent (cimetidine, methylprednisolone, epsilon-aminocaproic acid (EACA), or transaminomethyl cyclohexane carboxylic acid. PFN levels were measured by enzyme-linked immunosorbent assay at 0, 24, and 48 hours. Only endotoxin alone caused significant PFN elevation at 24 to 48 hours (p less than 0.01); however, its multiplicity of effects precludes localization of regulatory pathways. Methylprednisolone results in an accelerated rise in PFN levels after operation (p less than 0.05), probably through an intracellular augmentation PFN synthesis. EACA attenuates the postoperative response while transaminomethyl cyclohexane carboxylic acid augments the PFN rise. This effect of EACA implies the existence of a proteolytic fragment capable of stimulating PFN synthesis. If a nontoxic factor can be identified, the use of exogenous PFN may be avoided.

Aminocaproic Acid↗
PubMed1982

Observations on the effects of protease inhibitors on the suppression of experimental allergic encephalomyelitis.

Inhibitors of proteolytic enzymes were tested for their ability to suppress the clinical signs and CNS lesions produced by injection of purified myelin in complete Freund's adjuvant into Lewis rats. Pepstatin or a series of neutral protease inhibitors including aprotinin, soybean trypsin inhibitor, leupeptin, antipain, trans-aminomethyl cyclohexane carboxylic acid (AMCA), epsilon-amino caproic acid (EACA) nitrophenyl guanidino benzoate (NPGB), D- and L-polylysine, or a new commercial protease inhibitor, dipropionyl Rhein (DPR) were injected daily beginning on day 7 after immunization of rats with myelin. Aprotinin and soybean trypsin inhibitor exacerbated the symptoms and lesions of experimental allergic encephalomyelitis (EAE), leupeptin and antipain had no effect, and the plasminogen activators AMCA, EACA, NPGB, as well as poly-L- and poly-D-lysine and DPR suppressed various aspects of EAE. The measurement of acid protease as a biochemical method for quantitation of the degree of cellular infiltration into the CNS is proposed, and the results with the various treatments presented. AMCA and NPGB may exert their effects at the site of entrance of the lymphoid cells into the CNS.

Aminocaproic Acid↗
PubMed1994

Conformational studies of human plasminogen and plasminogen fragments: evidence for a novel third conformation of plasminogen.

The conformations of Glu-plasminogen and defined proteolytic fragments, in the presence and absence of 6-aminohexanoic acid (6-AHA), trans-4-(aminomethyl)cyclohexanecarboxylic acid (t-AMCHA), and benzamidine, were studied using three methods: size-exclusion high-performance liquid chromatography (SE-HPLC), small-angle X-ray scattering (SAXS), and dynamic laser light scattering (DLLS). The well-documented conformational change of Glu-plasminogen with 6-AHA or t-AMCHA was measured as a decrease in molecular elution time by SE-HPLC (8.93 +/- 0.01 to 8.32 +/- 0.01 min) and increases in radius of gyration (30.7 +/- 0.1 to 49.8 +/- 0.3 A) and Stokes radius (40.6 +/- 0.3 to 48.5 +/- 0.3 A) by SAXS and DLLS, respectively. The addition of benzamidine to Glu-plasminogen resulted in a conformation (radius of gyration 41.0 +/- 0.4 A and Stokes radius 46.6 +/- 0.3 A) distinct from that in the presence of 6-AHA. 6-AHA, but not benzamidine, induced significant conformational changes in Lys-plasminogen and kringles 1 + 2 + 3 + 4 + 5. We conclude that Glu-plasminogen adopts three distinct conformations involving two intramolecular interactions: one mediated by regions of the NH2-terminal peptide and kringle 5, competed for by 6-AHA or benzamidine, and the other possibly between kringles 3 and 4, competed for by 6-AHA but not benzamidine.

Aminocaproic Acid↗
PubMed1997

Prolonged arterial occlusion caused by thrombus development at sites of arterial bifurcation.

Although thrombogenic atheromas frequently develop at sites of arterial branching or bifurcation, the nature of such thrombus formation remains unclear. In this study, small rat mesenteric arteries (about 0.3 mm id) were observed using a video-microscope system. Exposure of the media by inducing compression damage over a short segment caused occlusive thrombus formation and subsequent spontaneous reperfusion repeatedly over about 30 min. Compression damage was induced either at a site just distal to the bifurcation (group 1, n = 7) or 5-10 mm downstream from the bifurcation (group 2, n = 7). The number of thrombotic occlusions was similar in the 2 groups, but the total duration of occlusion was significantly higher in group 1 (540 +/- 47 sec) than in group 2 (295 +/- 24 sec) (p < 0.01). The total duration of occlusion in group 1 was significantly reduced to 273 +/- 16 sec (p < 0.01) by mechanical interruption of flow in the other, intact, arterial branch. In the presence of blood flow through the intact branch, the occlusive thrombus at the bifurcation further enlarged in the direction of the intact branch, resulting in a significantly larger thrombus than in the absence of blood flow (17.1 +/- 2.1 vs 9.2 +/- 0.9 x 10(-2) mm2, p < 0.01). Stasis of the arterial blood per se did not affect the duration of thrombotic occlusion or increase plasma fibrinolytic activity. Thus, arterial occlusion caused by a thrombus arising at arterial bifurcations may be prolonged because of enlargement of the thrombus owing to the action of platelets in blood flowing through the intact branch.

Aminocaproic Acid↗
PubMedDate not supplied

Kasabach-kasabach-.

Giant haemangiomas combined with a haemostasis disorder of the Kasabach-Meritt type are rare and even more rare are the problems posed during labour when vulvo-vagino-uterine sites are involved. Two cases are reported. After summary of the clinical and biochemical studies, the authors report attempts to improve the haemostasis disorder, first with heparin and then with antifibrinolytic preparations, and to improve the angiomas with antifibrinolytic preparations in the hope of stimulating intrasacular thrombosis. In particular, the obstetric and surgical problems are discussed in the context of labour. In one case the outcome of labour was successful only moderate transfusion being required, and in the other the outcome was fatal despite the use of about 100 bottles of blood in the first 24 hours. In both cases the infants were normal.

Adult↗
PubMed1979

Protective effect of cetraxate, a new antiulcer drug, against serotonin-induced ulcer.

Cetraxate increased gastric mucosal blood flow and inhibited the decrease in blood content of the rat gastric preparation, as induced by serotonin. In addition, this compound decreased the inside pressure of the rat stomach and the tone of the rat fundus strip and inhibited the increase in gastric emptying rate induced by serotonin. Further effects of the drug were decrease in the tone of isolated rabbit aorta and inhibition of platelet aggregation as induced by thrombin. Decrease in the vascular resistance was apparently related to increase in the gastric blood flow. These experimental results suggest that the antiulcer effect of cetraxate is due to the improvement of blood circulation in the gastric mucosa.

Animals↗
PubMed1987

Antifibrinolytic therapy for prevention of hemorrhage during surgery of the thyroid gland.

The amount of fibrinolytic activity in the thyroid gland equals that of the prostate. In order to examine the effect of the antifibrinolytic drug tranexemic acid on perioperative bleeding saline or tranexemic acid were given randomized double blind to 76 consecutive patients who came for scheduled thyroid surgery. No significant differences were found in perioperative bleeding between patients in the treatment group (n = 39) and control group (n = 37).

Adenoma↗
PubMed1987

Suppression of clinical signs of cell-transferred experimental allergic encephalomyelitis and altered cerebrovascular permeability in Lewis rats treated with a plasminogen activator inhibitor.

The purpose of this study was to determine whether fibrinolysis resulting from activation of the clotting cascade in juxtaposition to endothelial cells of the central nervous system (CNS) microvasculature is important for development of clinical signs of experimental allergic encephalomyelitis (EAE) in recipient Lewis rats. Rats were injected with previously primed syngeneic lymph node cells, activated in vitro with guinea pig myelin basic protein, and subsequently treated daily with trans-4-(aminomethyl)cyclohexanecarboxylic acid (AMCA), a synthetic inhibitor of plasminogen activator. Clinical signs of EAE were significantly suppressed in AMCA-treated rats compared to saline-treated control recipient animals. Furthermore, suppression of clinical signs in AMCA-treated rats was accompanied by a significant curtailment in EAE-associated increased permeability of the blood-brain barrier (BBB). These findings provide evidence that CNS-associated deposition of fibrin and ensuing fibrinolysis, together with increased permeability of the BBB, are related prerequisite events for expression of clinical manifestations of EAE.

Animals↗