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At least 307 records · Page 17Linked to original sources
PubMed1975

ADP, thrombin, and Bothrops atrox thrombinlike enzyme in platelet-dependent fibrin retraction.

Clots formed upon the addition of thrombin to human platelet-rich plasma (PRP) retracted readily but the clotting enzyme from Bothrops atrox venom did not cause retraction in PRP unless ADP, collagen, epinephrine, or low concentrations of thrombin (0.1 U) were added. The latter type of retraction was inhibited by apyrase and creatine phosphate kinase in the presence of creatine phosphate, but that induced with higher concentration of thrombin (2 U) was not. In a system composed of washed human platelets and purified fibrinogen, Bothrops marajoensis (BM) thrombinlike enzyme (highly purified preparations of viper venom) did not cause clot retraction. Addition of ADP to the platelet-fibrinogen mixture prior to BM enzyme resulted in stimulation of clot retraction that could be dissociated from the release of platelet constituents. Addition of low concentrations of thrombin (0.1 U/ml) caused retraction associated with a considerable release of adenine nucleotides that was inhibited by potato apyrase. Electron micrographs showed platelet-fibrin aggregates in all types of retracted clots. Nonretracted clots formed in the presence of potato apyrase contained discoidal platelets that were not in close association with fibrin. It has been postulated that platelet-dependent fibrin clot retraction induced by collagen, epinephrine, and low concentration of thrombin is mediated by ADP. High concentrations of thormbin may possibly promote clot retraction independently of ADP.

Adenosine Diphosphate↗
PubMed2005

New treatment of neonatal pulmonary hemorrhage with hemocoagulase in addition to mechanical ventilation.

OBJECTIVE: To investigate the effect of a new treatment for neonatal pulmonary hemorrhage with hemocoagulase in addition to mechanical ventilation. METHODS: Forty-eight newborn infants with pulmonary hemorrhage were included and divided randomly into 2 groups. Among them, 28 patients were treated with hemocoagulase in addition to mechanical ventilation, and the other 20 neonates served as controls and were treated with mechanical ventilation only. RESULTS: Both the length of pulmonary hemorrhage and the duration of mechanical ventilation in the survivors were significantly shortened in the infants treated with hemocoagulase in addition to mechanical ventilation as compared to controls (p < 0.05). Moreover, all infants that were unable to remain in the neonatal intensive care unit died after discharge, and when their outcome was estimated as non-survivors, the mortality in the patients with this new treatment was 39.3% (11/28), which was significantly lower than in controls (75.0%, 15/20; p < 0.05). When the discharged infants were not included in the statistics, the mortality in the hemocoagulase group was 10.7% (3/28), which was also significantly lower than in controls (40.0%, 8/20; p < 0.05). CONCLUSIONS: The new treatment with hemocoagulase in addition to mechanical ventilation is effective in newborn infants with pulmonary hemorrhage.

Batroxobin↗
PubMed1975

Influence of cytotoxic drugs on platelet functions in vitro. III. Peptichemio.

The influence of Peptichemio (m-dichloroethyl-amino-l-phenyl-alanyl-peptide complex) on the following platelet functions was studied: aggregation, release of platelet factor 4, availability of platelet factor 3, acid phosphatases and reptilase clot retraction. Concentrations of the drug corresponding to that found in plasma of treated patients did not significantly influence platelet functions. Concentrations 10 times higher brought about an inhibition. It is concluded that after current dosage of Peptichemio, bleeding disorders caused by impairement of platelet functions are improbable.

Acid Phosphatase↗
PubMed1976

Interference on the haemostasis in dogs with induced coagulopathies by drugs affecting the platelet function.

Acetylsalicylic acid and phenylbutazone increased the bleeding significantly from standardized wounds in dogs defibrinogenated with Defibrase. Administration of dipyridamole and Xylocain had no effect. The results were the same in dogs treated with warfarin sodium. The results demonstrate the value of using laboratory animals with an induced coagulopathy when establishing the effect on the haemostasis exerted by drugs known in vitro to interfere with platelet functions. Acetylsalicylic acid and dipyridamole did not alter the activity of the K-vitamin-dependent coagulation factors, factors V, VIII, platelet count or fibrinogen concentration.

Afibrinogenemia↗
PubMed1975

Radioimmunoassay of human fibrinopeptide B and kinetics of fibrinopeptide cleavage by different enzymes.

Thrombin converts fibrinogen to fibrin monomer by cleaving fibrinopeptides A and B (FPA and FPB) from the amino terminal ends of the A (alpha) and B (beta) chains. A radioimmunoassay capable of measuring the A peptide in human blood as an index of thrombin action in vivo has been described previously. This paper describes the development of a radioimmunoassay for FPB and the use of both assays in the demonstration of distinctive patterns of cleavage of the amino terminal ends of the A (alha) and B (beta) chains of fibrinogen by various enzymes. Antisera were raised in rabbits to a synthetic analogue of FPB coupled to bovine serum albumin. FPB analogue was couple to desaminotyrosine and radiolabeled with 125I by the chloramine-T technique. The radiolabeled peptide was bound by the antiserum, and binding was inhibited by synthetic or native FPB. Unbound tracer was separated from bound tracer by charcoal adsorption. The senistivity of the assay was such that 50% inhibition of binding of the tracer was caused by 1.25 ng of the native FPB. Fibrinogen was treated with thrombin, plasmin, trypsin, Reptilase, and an extract of the venom from Ancistrodon contortrix contortrix (ACC). After ethanol precipitation and centrifugation, dialysates of enzymatically altered fibrinogen were assayed for FPA and FPB. The action of thrombin on fibrinogen resulted in a rapid release of FPA and a slower release of FPB. Plasmin cleaved a segment(s) of the B (beta) chain which included FPB but cleaved no detectable FPA-containing material for the first 2 h of incubation. In the case of plasmin-treated fibrinogen, the dialysates had been further treated with thrombin before being assayed for FPA and FPB. Trypsin rapidly cleaved both peptides, the B before the A. Reptilase cleaved only FPA in 24 h. ACC cleaved FPB at a rapid rate, with a slowere cleavage of FPA. The distinctive cleavage patterns produced by the serine proteases may be useful in interpreting the levels of FPA and FPB measured in human blood and in studying the generation of FPA and FPB in clinical blood samples.

Alpha-Globulins↗
PubMed1977

Dysfibrinogenemia associated with liver disease.

To test the possibility that a functionally abnormal fibrinogen may exist in some patients with liver disease, we studied the plasma and purified fibrinogens of five patients whose plasma thrombin times were prolonged at least 40% over normal controls. In no patient was there evidence of disseminated intravascular coagulation and/or fibrinolysis. No abnormalities were detected by immunoelectrophoresis of plasmas or purified fibrinogens. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of reduced patient fibrinogens showed normal mobility and amount of Aalpha, Bbeta, and gamma chains. Alkaline polyacrylamide gel electrophoresis and gradient elution, DEAE-cellulose chromatography of admixtures of radio-iodinated patient (125)I-fibrinogen and normal (131)I-fibrinogen showed identical mobility in the gel and simultaneous elution from the column, respectively. Thrombin and Reptilase (Abbott Scientific Products Div., Abbott Laboratories, South Pasadena, Calif.) times of purified patient fibrinogens were prolonged, and calcium ions improved but did not completely correct these defects. Increasing amounts of thrombin progressively shortened the clotting times of patient fibrinogens but not to the level of normal. Addition of equal amounts of patient fibrinogen to normal fibrinogen resulted in a prolongation of the thrombin time of the normal protein. Thrombin-induced fibrinopeptide release was normal. Fibrin monomers prepared from patient plasmas and purified fibrinogens demonstrated impaired aggregation at low (0.12) and high (0.24) ionic strength. These studies demonstrate that some patients with liver disease and prolonged plasma thrombin times have a dysfibrinogenemia functionally characterized by an abnormality of fibrin monomer polymerization.

Alcoholism↗
PubMed1992

Endothelial cell spreading on fibrin requires fibrinopeptide B cleavage and amino acid residues 15-42 of the beta chain.

Adhesion and spreading of cultured human umbilical vein endothelial cells on fibrin surfaces of varying structure were characterized to understand better the interactions occurring between endothelium and fibrin at sites of vascular injury. Fibrin prepared with reptilase, which cleaves only fibrinopeptide A from fibrinogen, and fibrin prepared with thrombin, which cleaves both fibrinopeptide A and fibrinopeptide B, equally supported endothelial cell adhesion. In contrast, only fibrin made with thrombin mediated endothelial cell spreading, as assessed by fluorescence microscopy of cells stained with rhodamine phalloidin to identify actin stress fibers or by scanning electron microscopy. Fibrin prepared with reptilase failed to support cell spreading. To further investigate the role of the amino terminus of the fibrin beta chain after fibrinopeptide B cleavage in promoting cell spreading, protease III from Crotalus atrox venom was used to specifically cleave the amino-terminal 42 residues of the fibrinogen B beta chain. After clotting with thrombin, this fibrin derivative lacking B beta 1-42 failed to support significant cell spreading. Spreading on fibrin was unaffected by depletion of Weibel-Palade bodies from endothelial cells, indicating that the spreading was independent of stimulated von Willebrand factor release. We conclude that endothelial cell spreading on fibrin requires fibrinopeptide B cleavage and involves residues 15-42 of the fibrin beta chain.

Batroxobin↗
PubMedDate not supplied

Evaluation of kits for the detection of fibrin(ogen) degradation products in dogs.

The sensitivities and specificities of 3 commercial serum fibrin(ogen) degradation product (FDP) kits and 1 plasma FDP kit for the detection of FDPs in dogs were determined. Blood was collected for measurement of serum and plasma FDP concentrations from 30 healthy dogs and from 20 dogs that fulfilled clinical and laboratory criteria for disseminated intravascular coagulation. To determine the effect of hemolysis on FDP results, blood was collected simultaneously into Bothrops atrox venom-based and thrombin-based serum collection tubes for measurement of FDPs using a single serum FDP kit. The sensitivity (80-95%) and specificity (90-100%) for a positive or negative FDP result, regardless of concentration, was similar for all kits. Kits yielded discordant results in individual dogs and FDP concentrations obtained from 1 serum FDP kit were consistently higher than those from the other kits. Serum prepared from venom-based collection tubes was significantly more hemolyzed than serum prepared from thrombin-based collection tubes or citrated plasma. Hemolysis did not affect the FDP results. On the basis of these results, we conclude that commercial latex agglutination kits for detection of FDPs in serum and plasma samples from human patients are valid for use in dogs. The plasma FDP assay is a viable alternative to currently used serum FDP assays and has the advantage of using a single (citrated plasma) sample for measuring coagulation parameters and FDP concentration.

Animals↗
PubMed1991

Chronological study of recovery of sudden deafness treated with defibrinogenation and steroid therapies.

The time courses of hearing recovery resulting from two types of treatment of sudden deafness patients, defibrinogenation (DF) therapy and betamethazone (BM) therapy, were analyzed and compared. A paired double-blind comparative study was performed on 168 patients. The average hearing level was 79.2 dBHL in the DF therapy group (n = 82) and 82.3 dBHL in the BM therapy group (n = 86). The DF group showed significantly better hearing 1 week after start of treatment at frequencies of 0.25, 0.5 and 1 kHz. After 2 weeks of treatment, the average hearing level for the frequency range of 0.25-4 kHz was 47.0 dBHL with DF therapy and 55.8 dBHL with BM therapy. Thus, the DF group still showed better hearing than the BM group (p less than 0.10, t-test), but not as significantly as after 1 week. It is concluded that therapy for increasing blood circulation is important in the early phase of sudden deafness, especially for hearing loss in the low to middle frequency range.

Analysis of Variance↗
PubMed1976

Anticoagulation with defibrase during prolonged extracorporeal circulation in the dog.

Defĩbrase was used for anticoagulation in dogs during extracorporeal perfusion up to 6 hours with a Travenol membrane oxygenator or a Pall filter. The anticoagulation effect was adequate. The already low fibrinogen concentration became unmeasurable, the platelet count decreased, and the fibrin(ogen) degradation products increased during the perfusion. Histological examination showed platelets and white blood cells on the membranes. Perfusion pressure and blood flow were stable during the experiments, and no bleeding, thromboembolism or other adverse side-effects were noted. Defibrase might be an alternative to heparin for anticoagulation during extra-corporeal circulation.

Animals↗
PubMed1976

Fibrin clot retraction by human skin fibroblasts: effects of ADP and thrombin.

Thrombin stimulated human skin fibroblasts to retract fibrin clots. When Bothrops marajoensis thrombinlike enzyme was substituted for thrombin, no retraction occurred. Fibroblasts were found to contain 12 nmole of ATP and 3.6 nmole of ADP/mg of protein, a value closely resembling that of nonmetabolic adenine nucleotides in platelets. Thrombin caused neither release of adenine nucleotides from the suspension of fibroblasts harvested enzymatically nor did addition of ADP stimulate fibroblasts to retract fibrin clots.

Adenosine Diphosphate↗