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PubMed1986

The interaction of the factor VIII/von Willebrand factor complex with hematin.

Intravenous infusion of hematin, used in the treatment of acute porphyria, induces a decline in the plasma factor VIII/von Willebrand factor complex (VIII/vWF) and thrombocytopenia. We investigated this problem by studying the interaction between hematin, purified VIII/vWF, and platelets in vitro. Hematin was labeled with either 59Fe or 3H and characterized by gel chromatography. Hematin self-aggregated, forming a complex with an average molecular weight of approximately 10,000 daltons. When incubated with VIII/vWF for 30 min at 37 degrees C and applied to Sepharose CL-4B, the hematin eluted with the VIII/vWF in the void volume. Hematin inhibited the dissociation of factor VIII antigen (VIII:Ag) from the von Willebrand antigen (vWF:Ag) in 0.25 M CaCl2, and reversed the aggregation of VIII:Ag induced by 0.1 M 6-aminocaproic acid. Both hematin and the hematin-VIII/vWF complex bound to washed normal platelets and to platelets from a patient with Bernard-Soulier syndrome. Thrombasthenic platelets were not aggregatable by hematin, and bound significantly less hematin-VIII/vWF than normal platelets suggesting that hematin-induced platelet activation was required for binding. Likewise, binding was inhibited by PGE1 which also prevented aggregation. We conclude that hematin forms complexes with VIII/vWF, alters the functional activity and dissociation of this compound, and participates in the binding of VIII/vWF to platelets.

Blood Platelets↗
PubMed1987

Extracellular matrix of cultured bovine aortic endothelial cells contains functionally active type 1 plasminogen activator inhibitor.

The extracellular matrix (ECM) of cultured bovine aortic endothelial cells (BAEs) was analyzed by immunoblotting and reverse fibrin autography and shown to contain type 1 plasminogen activator inhibitor (PAI-1). Most PAI-1 in the ECM formed complexes with exogenously added tissue-type plasminogen activator (tPA), demonstrating that this PAI-1 was functionally active. The resulting tPA/PAI-1 complexes were recovered in the reaction solution, indicating that the PAI-1 in such complexes no longer bound to ECM. The PAI-1 could not be removed by incubating ECM in high salt (2 mol/L NaCl), sugars (1 mol/L galactose, 1 mol/L mannose), glycosaminoglycans (10 mmol/L heparin, 10 mmol/L dermatan sulfate), or epsilon-aminocaproic acid (0.1 mol/L). However, PAI-1 could be extracted from ECM by treatment with either arginine (0.5 mol/L) or potassium thiocyanate (2 mol/L), or by incubation under acidic conditions (pH 2.5). ECM depleted of PAI-1 by acid extraction was able to bind both the active and latent forms of PAI-1. In this instance, most of the bound PAI-1 did not form complexes with tPA, indicating that the latent form was not activated as a consequence of binding to ECM. Although the PAI-1 activity in conditioned medium decayed with a half-life (t 1/2) of less than 3 hours, the t 1/2 of ECM-associated PAI-1 was greater than 24 hours. These data suggest that PAI-1 is produced by cultured BAEs in an active form and is then either released into the medium where it is rapidly inactivated or into the subendothelium where it binds to ECM. The specific binding of PAI-1 to ECM protects it from this inactivation.

Animals↗
PubMed1985

[Fulminant and gradual evolution of the clinical manifestations of lumbar osteochondrosis].

A vertebroneurological examination of 187 patients with lumbar osteochondritis revealed the presence of two variants of its exacerbation: fulminant (occurring within 1-3 days) and gradual (with a longer period of progress). The fulminant variant was associated with tension of the cellular immunity expressed in a decreased index of leukocyte migration inhibition and the corresponding therapeutic effect of epsilon-aminocaproic acid.

Acetylcholine↗
PubMed1988

[Binding of lys-plasminogen to E-fragment of fibrinogen].

The interaction of Lys-plasminogen and its fragments with fibrinogen fragment E was studied by equilibrium affinity binding. A quantitative analysis of binding parameters revealed two types of binding sites responsible for Lys-plasminogen interaction with the immobilized fragment E, i.e., with a high (Kd = 1.5 x 10(-6) M) and low (Kd = 82 x 10(-6) M) affinity ones. Among plasminogen fragments, only miniplasminogen and KI-3 bound immobilized fragment E and were eluted by epsilon-aminocaproic acid. Hence, two lysine binding sites may be involved in the binding of Lys-plasminogen to fragment E; they are localized in the KI-3 and K5 kringle structures.

Chromatography, Gel↗
PubMedDate not supplied

[Participation of the proteolysis system in promoting the virulence of the influenza virus and development of the infectious process; the antiviral effect of protease inhibitors].

The results of the authors' own studies and data from the literature attesting to an important role of proteolytic mechanisms in influenza virus physiology and the development of the infectious process are summarized. The etiotropic and pathogenetic effectiveness of proteolysis inhibitors in influenza was demonstrated experimentally and clinically. Data are presented on the immunostimulating and prophylactic effect of a proteolysis inhibitor, E-aminocaproic acid. It is concluded that the use of proteolysis inhibitors in viral infections holds good promise.

Animals↗
PubMed1988

Bed rest versus activity ad lib in the treatment of small hyphemas.

The management of small hyphemas remains controversial. Some authors advocate hospitalization, strict bed rest, and medical therapy with aminocaproic acid. Others are less conservative and recommend treatment on an ambulatory basis without the drug. In order to establish the overall rebleed rate for small hyphemas and to assess whether or not strict bed rest improves the prognosis, we studied 73 patients with small hyphemas occupying less than one third of the anterior chamber. Thirty-seven patients, during the first year of the study, were hospitalized and treated with strict bed rest while 36 patients, during the second year, were hospitalized but allowed to ambulate freely. The overall incidence of rebleeds was 15% (11 of 73). The incidence of rebleeds and other complications was not statistically different between the two study groups. Additionally, the final visual acuity in both groups was essentially identical. We conclude that bed rest does not improve the prognosis in cases of small hyphemas.

Atropine↗
PubMed1986

Chemotactic peptides modulate adherence of human polymorphonuclear leukocytes to monolayers of cultured endothelial cells.

We have used a new centrifugation assay to examine the effects of highly purified human C5a and C5a des Arg, as well as effects of N-formyl-methionyl-leucyl-phenylalanine (FMLP), on both the extent and strength of human polymorphonuclear leukocyte (PMN) adherence to monolayers of cultured human umbilical vein endothelial cells. At concentrations that were chemotactic for PMN, C5a (0.1 nM), C5a des Arg (5.0 nM), and FMLP (1.0 nM) significantly reduced the percentage of PMN that adhered to endothelial monolayers. Adherence also was reduced by C5a des Arg that was generated by incubating (37 degrees C, 30 min) fresh human serum with either zymosan or purified C5a. High concentrations of C5a (greater than 1.0 nM) and FMLP (greater than 50 nM) that diminished PMN chemotaxis significantly enhanced the percentage of PMN that adhered tightly to endothelial cells (adherent cells resisted a dislodgment force of 1200 X G). Tight adherence of PMN to endothelial cells also was increased by high concentrations of C5a that were added to human serum in which carboxypeptidase N activity was destroyed by heating (56 degrees C, 30 min), and by C5a that was generated by incubating (37 degrees C, 30 min) fresh human serum with zymosan in the presence of the carboxypeptidase N inhibitor, epsilon-aminocaproic acid. High concentrations of C5a des Arg (up to 80 nM) neither enhanced adherence of PMN to endothelial cells nor decreased PMN migration. Thus, a reciprocal relation exists between PMN migration and PMN adherence to endothelial cells in response to chemotactic factors. At concentrations that are chemotactic for human PMN, C5-derived peptides and FMLP reduce the adherence of PMN to endothelial monolayers. Only at concentrations that decrease PMN migration do C5a and FMLP augment PMN adherence.

Adult↗
PubMed1987

[Roentgeno-endovascular occlusion as a method of hemostasis in abdominal trauma].

Under analysis is the authors' experience with roentgen-endovascular occlusions (REO) in 18 patients with closed injuries of the abdomen with massive hemorrhage. The embolization of spleen vessels was made in 8 patients, hepatic vessels--in 5 patients, renal vessels--in 3 patients and iliac artery branches--in 2 patients. In 10 cases REO was used as an independent method for arrest of hemorrhage and in 8 patients--for the preoperative preparation of the patients. The home hemostatic sponge was used in combination with superselective administration of the aminocaproic acid as the embolizing material.

Abdominal Injuries↗
PubMedDate not supplied

[Hydrocephalus following subarachnoid hemorrhage].

The authors present 56 patients with subarachnoid haemorrhages in whom CT of the head demonstrated internal hydrocephalus. This complication was observed most frequently in the age group 51-60 years. In 39% of cases hydrocephalus was low grade, in 36% it was moderately severe, and in 25% high grade. In 33 patients (59%) a syndrome of clinical symptoms and signs was observed which could be related, in part at least, to hydrocephalus. In 11% of cases. Pudenz valve had to be implanted. No significant differences were found in the frequency of hydrocephalus in late period after subarachnoid haemorrhage in relation to sex, number of haemorrhages, clinical state, vasospasm, treatment with epsilon-aminocaproic acid and dexamethasone.

Adolescent↗
PubMedDate not supplied

Liquid chromatographic determination of taurine in vitamin premix formulations.

A liquid chromatographic (LC) method is described for the determination of taurine in vitamin and vitamin-mineral premix formulations. The method involves extraction of taurine with 0.1 M bicarbonate buffer, followed by precolumn derivatization with dansyl chloride and LC using fluorescence detection. 6-Aminocaproic acid is used as an internal standard. A reverse phase analytical column and a mobile phase of 0.1 M acetate buffer solution (pH 7.2)-acetonitrile (75 + 25) are used. Vitamins, minerals, and other excipients in the premix formulations do not interfere in the determination. The method is simple, precise, and accurate.

Chemistry, Pharmaceutical↗
PubMed1986

Binding of plasminogen to cultured human endothelial cells.

Endothelial cells are known to release the two major forms of plasminogen activator, tissue plasminogen activator (TPA) and urokinase. We have previously demonstrated that plasminogen (PLG) immobilized on various surfaces forms a substrate for efficient conversion to plasmin by TPA (Silverstein, R. L., Nachman, R. L., Leung, L. L. K., and Harpel, P. C. (1985) J. Biol. Chem. 260, 10346-10352). We now report the binding of human PLG to cultured human umbilical vein endothelial cell (HUVEC) monolayers, utilizing a newly devised cell monolayer enzyme-linked immunosorbent assay system. PLG binding to HUVEC was concentration dependent and saturable at physiologic PLG concentration (2 microM). Binding of PLG was 70-80% inhibited by 10 mM epsilon-aminocaproic acid, suggesting that it is largely mediated by the lysine-binding sites of PLG. PLG bound at an intermediate level to human fibroblasts, poorly to human smooth muscle cells, and not at all to bovine smooth muscle or bovine endothelial cells; unrelated proteins such as human albumin and IgG failed to bind HUVEC. PLG binding to HUVEC was rapid, reaching a steady state within 20 min, and quickly reversible. 125I-PLG bound to HUVEC with an estimated Kd of 310 +/- 235 nM (S.E.); each cell contained 1,400,000 +/- 1,000,000 (S.E.) binding sites. Functional studies demonstrated that HUVEC-bound PLG is activatable by TPA according to Michaelis-Menten kinetics (Km, 5.9 nM). Importantly, surface-bound PLG was activated with a 12.7-fold greater catalytic efficiency than fluid phase PLG. These results indicate that PLG binds to HUVEC in a specific and functional manner. Binding of PLG to endothelial cells may play a pivotal role in modulating thrombotic events at the vessel surface.

Animals↗
PubMed1986

[Early surgery of intracranial aneurysms].

In spite of scientific progress during the last two decades, microsurgery, neuroanesthesiology, and a better knowledge of the pathophysiology of cerebral vasospasm, the outcome of subarachnoid hemorrhage (S.A.H.) patients remains very poor. Each year, 28,000 North Americans are afflicted. Eighteen thousand of these patients will either die or become severely debilitated, a mortality morbidity of 64%. Only one patient out of five may return to the premorbid state. International cooperative studies report that the highest rate of rebleeding occurs during the first 24 hours post S.A.H. There is no rebound phenomenon during the 7th-8th day post S.A.H. Cerebral vasospasm begins during the 2d-4th day post S.A.H. and reaches its peak around the 8th day post bleed. Antifibrinolytics like AMICAR (aminocaproic acid) do not reduce significantly the rebleeding rate. In most of the cases the therapeutic level of these drugs is reached only on the third or fourth day of treatment. Hence antifibrinolytics are inactive during the first crucial seventy two hours. Antifibrinolytics increase the incidence of vasospasm, hydrocephalus, and thromboembolic phenomenon. At Infant Jesus Hospital, Quebec City, S.A.H. patients are operated on early since more than two years. Patients included in this study were admitted between January 1983 and December 1984. One hundred and thirty six patients were operated upon, 22 patients operated on acutely, less than 72 hours post S.A.H. Evaluation of these patients included the Glasgow Coma Scale (G.C.S.), the grade according to Botterell classification, a CT Scan, and angiography. A preoperative evaluation included Botterell classification and G.C.S., a post operative evaluation was performed during the first and seventh post operative days.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1979

Investigation of cholecystokinin-octapeptide splitting enzyme in dog kidney.

In vitro experiments were carried out to examine the enzymatic activity in various organ homogenates of the dog, which inactivates the biological activity of the synthetic cholecystokinin-octapeptide (CCK-OP). The highest splitting activity was found in the renal cortex; substantially lower activities were registered in the lung, pancreas and small intestine. It seems interesting that neither the gallbladder nor the saliva and the serum contained measurable amount of the CCK-OP splitting activity. An effort was made to characterize the CCK-OP inactivating principle found in the renal cortex. It was ascertained that the CCK-OP was inactivated by a peptidase which is heat sensitive, has a pH optimum of 7,4 and could be inhibited by chelating agents (EDTA) and epsilon-aminocaproic acid. The fact that most of the enzyme function is associated with the sediment obtained at 12 000 g speaks in favour of its mitochondrial origin.

Animals↗
PubMed1980

[Mechanism of action of certain fibrinolytic bis-tetrahydroisoquinolines: their antagonists and histamine- and 5-hydroxytryptamine-releasing effects (author's transl)].

1, 1'-Heptamethylene-bis-6, 7-dimethoxy-1, 2, 3, 4-tetrahydroisoquinoline (HBDT) and 1, 1'-tetramethylene-bis-6, 7-dimethoxy-1, 2, 3, 4-tetrahydroisoquinoline (bisobrin) produced an edema when given subcutaneously into the hind paws of rats. The inhibitory effects of various antagonists on the paw edema and fibrinolysis induced by HBDT were examined in rats to determine whether chemical mediators other than histamine were involved. The relation of histamine to the fibrinolytic activity of these bis-tetrahydroisoquinoline derivatives has already been reported. Both edema and fibrinolysis were significantly inhibited by pretreatment with promethazine, cyproheptadine or phentolamine, but not by dibenamine, propranolol, atropine, indomethacin or pyridinolcarbamate. epsilon-Aminocaproic acid inhibited the fibrinolytic activity completely without any effect on the paw edema. HBDT released 5-hydroxytryptamine (5-HT) along with histamine from rat peritoneal mast cells. However, the amount of released 5-HT was considerably smaller than that of histamine. These results suggested that bis-tetrahydroisoquinolines released both histamine and 5-HT and that these mediators produced paw edema and induced fibrinolysis by enhancement of plasmin production.

Animals↗
PubMed1976

[Fibrinolytic properties of a heparin-ocrase complex].

The obtained heparin-ocrase complex includes properties of inhibiting coagulation and a high fibrinolytic activity in vitro and in vivo. The fibrinolytic activity of the heparin-ocrase complex is higher than the equivalent amount of ocrase. The fibrinolytic activity of the complex is not only evident on non-stabilized fibrin plates, but likewise on stabilized ones and at the presence of inhibitors of enzymatic fibrinolysis, such as Trasylol and epsilon-aminocaproic acid. The complex formation between heparin and protease was confirmed by means of cross-paper electrophoresis and spectrophotometry.

Anticoagulants↗
PubMed1981

[Fibrinogen and plantar edema induced by lambda carrageenan].

1. Batroxobine which induces fibrinogen consumption, accelerates the development of 48/80 and lambda carrageenan oedema: in the rat the various products released from fibrinogen and fibrin increase these inflammatory reactions. 2. Heparin and epsilon-aminocaproic acid have no influence on carrageenan oedema: the derivatives of fibrinogen do not take part in the constitution of the inflammatory reaction induced by carrageenan. 3. The anti-inflammatory action of this sulfated polygalactose does not depend on its anti-coagulant activity.

Animals↗
PubMed1984

Splenectomy in onyalai. A report on 5 cases.

Onyalai is an acquired immune thrombocytopenia with 10% mortality. Conservative measures such as traditional medicines, corticosteroids and blood transfusion have not always controlled severe bleeding or prevented death. Five patients (2 male, 3 female) with onyalai who had uncontrollable haemorrhage, thrombocytopenia and documented previous attacks of severe bleeding, underwent splenectomy. The patients were screened for malaria, sickle-cell anaemia and bilharzia. Vitamin K and epsilon-aminocaproic acid were administered pre-operatively, and fresh blood was given during surgery. The duration of follow-up varied between 280 and 544 days. There were no operative complications. Bleeding stopped in all patients and the platelet counts increased within 24 hours. All achieved normal platelet counts, but these were not always sustained. Three patients remained free of disease with normal platelet counts up to days 539, 539 and 544 of follow-up. Two patients had a recurrence of bleeding and died from cerebral haemorrhage and haemorrhagic shock.

Adolescent↗