bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Reaction between Prothombin and Staphylocoagulase
Authors: Hemker H. C. , Muller A. D. , Bas B. M. 
Published: June 2019

The reaction between prothrombin and staphylocoagulase is studied.a. Optimal amounts of the active reaction product (coagulase-thrombin) are found when equimolar amounts of prothrombin and staphylocoagulase are added together.b. The molecular weight of coagulase-thrombin equals the sum of the molecular weights of staphylocoagulase and prothrombin, both when estimated by gelfiltration and by SDS-polyacrylamide gel electrophoresis.c. The amino acid composition of coagulase-thrombin is not in contrast with the sum of the amino acid compositions of staphylocoagulase and prothrombin.d. In a preparation of coagulase-thrombin the N-terminal amino acids are those of prothrombin (alanine) and staphylocoagulase (aspartic acid).e. An antibody against coagulase-thrombin precipitates both prothrombin and staphylocoagulase but not thrombin.f. It is concluded that the thrombin acitivity in coagulase-thrombin is a result from a stoichiometric reaction between one molecule of prothrombin and one molecule of staphylocoagulase and that limited proteolysis does not play a role in this mechanism.
Role of Trisodium Citrate in the Unclottability by Thrombin of Fibrinogen Metz
Authors: Soria C. , Soria J. , Samama M. , Poirot E. , Kling G. 
Published: June 2019

In a case of homozygous dysfibrinogenemia, the whole blood clotting time was moderately prolonged, while the thrombin clotting time was infinite, whatever dose or nature of thrombin used. Besides, the bleeding syndrome in this case was very weak.We observed also that only after trisodium citrate addition to purified fibrinogen, the abnormal fibrinogen became unclottable by thrombin even after addition of calcium chloride, since without trisodium citrate thrombin time was only prolonged.By immunoelectrophoresis and by isofocusing in the presence or in the absence of trisodium citrate, we therefore undertook to show that trisodium citrate reacts more strongly with the abnormal fibrinogen than with normal one. Thus, trisodium citrate conferring a negative charge to the pathological molecule, the abnormal fibrinogen became resistant to clotting with thrombin. Protamine sulfate, by positiving the charges of fibrinogen, partially corrects the defect in fibrin formation.
Release of Platelet Factor 4 (PF 4) During Repeatedly Induced Platelet Aggregation in Vivo
Authors: Vaage J. , Gjesdal K. 
Published: June 2019

After induced intravascular platelet aggregation a pulmonary vasoconstriction occurs due to the release of vasoactive substances from platelets (Acta physiol. scand. 92, 546-556, 1974). PF 4 has been suggested to be a marker of the platelet release reaction. In the present experiments the release of PF 4 and the vasoactive effects of induced platelet aggregation were compared in cats.Successive i. v. infusions of either ADP or collagen were given to induce platelet aggregation. The plasma level of PF 4 was measured by electroimmuno assay immediately before each infusion and at the maximal ensuing lung response. The initial infusion of either ADP or collagen increased PF 4 in plasma by about 25%. After several ADP-infusions neither lung responses nor PF 4 release could be elicited by further infusions, although reversible aggregation of platelets was still induced. At this stage collagen infusions gave profound lung responses, but no release of PF 4. Another group of animals were given 3 successive collagen infusions. The lung responses were similar after each infusion, but the release of PF 4 became gradually reduced.These data suggest that the release of PF 4 from platelets is dissociated from that of the vasoactive agents.
On the Action of Intravenously Applied Acetylsalicylic Acid (ASA) on Platelet Functions, a Kinetic Study
Authors: Loew D. , Vinazzer H. 
Published: June 2019

There is general agreement that ASA inhibits platelet aggregation, adhesion and release reactions when given orally. In the present study, 10 individuals received a single intravenous dose of 500 mg ASA to examine the kinetics of the influence on platelet functions. Blood was drawn prior to ASA and at intervals between 2 minutes and 72 hours after injection.Collagen induced platelet aggregation as well as PF 3 and PF 4 release started to decrease 2 minutes after ASA and reached a minimum after 1 hour. A full ASA effect could still be observed after 24 hours though ASA had disappeared from plasma by that time. Simultaneously, in-vitro examinations with ASA were carried out. ASA was added to fresh platelet rich plasma in a concentration correspondent to the in-vivo dose. The inhibition of platelet aggregation and PF 4 release had a lag time of 1 hour and was considerably less distinct than in vivo. No inhibition of PF 3 release could be observed. The results demonstrate a rapid action of ASA when given intravenously while the in-vitro effect is much less distinct. A probable explanation is a direct effect of ASA on the platelet membrane. The enhancement in vivo is supposed to be caused by splitting of the acetylic group from ASA.
Thrombinaemia and Hematological Changes Induced in Dogs by the Artificial Kidney
Authors: Veenhof C. H. N. , Prakke E. M. , Vreeken J. , Bosch E. , Meer J. van der 
Published: June 2019

The aim of the investigation was 1) to trace the chronological sequence of coagulation events and haematological changes induced by the artificial kidney and the reaction of the living organism; and 2) to study the influence of various drugs.Group A, non-treated: in the venous blood factor V activity and fibrinopeptide A, generated in vitro, reached maximal values at 15 min. At 10-15 min fibrinomonomers were detected. From 15 min onwards FDP appeared. Granulocyte and platelet counts reached very low values at 10-15 min. The concentration of serotonin (5HT) was maximal at 10—15 min.Group B : heparin and coumarin prevented thrombin activity. However, they did not inhibit the initial fall of leucocytes and platelets. Release of 5HT did not occur when no thrombin activity was detected.Group C, treated with Acetylic Salicylic Acid (ASA), sulfinpyrazon, dipyridamol in combination with ASA, polyphloretinphosphate : thrombin generation was postponed to a small degree. However, the initial loss of leucocytes and platelets was not diminished. The release of 5HT was reduced.In all three groups the manifestations of thrombin activity were much less pronounced in the arterial line indicating a clearing mechanism in the body. The FDP values in the arterial blood were not different from those on the venous side. The initial decrease of leucocyte and platelet counts, especially in the arterial side suggests trapping in the body. Moreover, the arterial-venous difference in platelet counts indicates retention of platelets in the extracorporeal circuit. The drugs used prevented or diminished generation of thrombin. To influence the initial decrease in leucocyte and platelet counts attention should be directed more to the properties of the different elements of an artificial kidney than to the blood components.
The Photometric Aggregation Test (PAT III). A Screening Test for Enhanced Platelet Aggregation
Authors: Krzywanek H. J. , Breddin K. 
Published: June 2019

PAT III has been developed for the photometric registration of “spontaneous” platelet aggregation. Citrated PRP is rotated at 20 rpm and 37° C using a disc shaped polystyrol cuvette. Aggregation inducing substances are not used. Changes in optical density which occur when platelets aggregate, are registered on a chart recorder.The following parameters are of special interest : Tr = time from start of rotation to onset of aggregation; angle alpha2 as a measure of max. aggregation speed; and α2/Tr. These parameters allow a more precise differentiation of the spontaneous platelet aggregation.Our previous findings with PAT I were confirmed by our recent studies: In 124 normal subjects we found a gradual decrease of missing spontaneous aggregation (α 0-40°) with rising age, whereas the number of persons with enhanced aggregation (α 41-90°) reached 70-80% beyond the age of 50. The percentage of 183 patients with diabetes mellitus and enhanced platelet aggregation was greater than that of age matched controls.
Automated Monitoring of Platelet Aggregation in Multiple Samples of whole Blood
Authors: Clarke N. , McCabe V. 
Published: June 2019

Whole blood may be first agitated in a circular transparent rotor chamber, and then rotated continuously to produce plasma/red cell separation for monitoring. The rotor is driven by a low inertia, printed circuit d.c. motor (108 Watt) which is automatically controlled. The pattern of rotation is determined by a signal generator which provides various waveforms at adjustable frequencies and also at fixed speeds.By segmenting the rotor into multiple cuvettes (Vol = 0.4 ml) it is possible to monitor the platelet concentration, after agitation, as each cuvette spins through the stationary optical system. This consists of a light-emitting diode (peak: 900 nm), pulsed at 10 kHz in order to eliminate ambient light effects, and a photodetector with a built-in amplifier, fed to an amplifying circuit which eliminates other signals. An electronic circuit permits selection of the signal from each cuvette on a direct reading meter. Cuvette No. 1 is identified by a photocell-detector trigger.Platelet-free plasma is about zero O. D. in the infra red with respect to a water blank, and with attention to specific criteria such as optical geometry and light path, platelet concentration may be accurately determined.
Determination of Fibrinmonomer (FM) from Plasma by Affinity Chromatography on Insolubilized Fibrinogen (FG-ag)
Authors: Matthias F. R. , Reinicke R. , Heene D. L. , Lasch H. G. 
Published: June 2019

Quantitative estimation of soluble fibrinmonomer in plasma may be achieved by affinity chromatography on insolubilized fibrinogen (FG-ag), as described by us (Heene, Matthias: Thrombosis Res. 2, 137, 1973). The procedure is based on the reversible adsorption of fibrinmonomer to FG-ag. Column: 0.9 × 28 cm FG-ag; sample volume: 2 ml plasma; adsorption buffer A: 0.05 M tris-H3PO4, 0.1 M NaCl, 0.001 M TAME, 0.005 M EDTA, 100 KIU Trasylol/ml, pH 7.8 ; desorption buffer B : 0.05 M tris-H3P04, 2 M NaBr, 0.001 M TAME, 0.005 M EDTA, 100 KIU Trasylol/ml, pH 5.3. Determination of fibrinmonomer from peak B was performed by the staphylococcal clumping test. The experimental conditions were standardized for a quantitative evaluation by use of radioactive labelled fibrinogen and fibrinmonomer.Besides normal samples plasma of patients with consumption-coagulopathy, acute myocardial infarction and with carcinomas were investigated. The elevation of fibrinmonomer in plasma was dependent on the severity of the disease. In many cases an elevation of fibrinmonomer was found even before the analysis of clotting factors or the ethanol test indicated hypercoagulability or consumption-coagulopathy. Under conditions of an increased turn-over of clotting factors it is possible to follow up quantitatively changes in the concentration of fibrinmonomer in plasma during the course of the disease.
Improvement of the Preparation of Factor VIII Concentrates
Authors: Vermeer C. , Soute B.A.M. , Brummelhuis H. G. J. 
Published: June 2019

The effect of some variables on the yield of factor VIII procoagulant activity during the preparation of factor VIII concentrates was investigated. The results may be summarized as follows:- The pH of the anticoagulant solution, which results in an optimal recovery of factor VIII in plasma varies with the time, during which the blood or plasma has to be stored before the plasma is frozen. The temperature during the storage of blood and plasma should be higher than 10° C.- A high freezing and thawing rate of the plasma results in a high recovery of factor VIII and less contaminating proteins and lipids in the cryoprecipitate.- After centrifugation and dissolving of the precipitate, the preparation may be lyophilized. An appreciable loss of activity is found when the temperature during this process exceeds 20° C.- From the cryoprecipitate factor VIII can be further purified by precipitation with PEG 4000. The fraction between 2½% at 20° C and 6% at 0° C was used. Within certain limits this precipitation is independent on the protein concentration, pH, time, and ionic strength. Mandelate (0.3% w/v) prevents irreversible precipitation of fibrinogen during all operations.- Sterilization of the dissolved precipitate was achieved by filtration through membrane filters (0.3 μ) on which the filter aids Celite 535 and Hyflo supercel were layered.- PEG precipitation and sterilization induce a 20% loss.- The clinical use of the product was assayed in series of infusions in hemophiliacs.
Platelet Phospholipid Synthesis During” Thrombin-Induced Platelet Aggregation
Authors: Kaulen H. D. , Gross R. 
Published: June 2019

To study the effect of aggregation and release on platelet membrane metabolism human platelet phospholipids were labeled with either glycerol-C 14 or P 32. After washing off the residual label in order to avoid interference of aggregation with uptake, the changes in the distribution of the label in the various phospholipid classes were followed during the first four minutes of thrombin-induced aggregation. Glycerol-C 14 was incorporated into all glycerophospholipids except the polyphosphoinositides, indicating the various rates of de-novo phospholipid synthesis, and this incorporation was not changed by aggregation. P 32, labeling preferentially the phosphoinositides, was rapidly incorporated over non-aggregated controls in the course of aggregation from water-soluble precursors into phosphatidic acid, di- and triphosphoinositide ositide. As no new de-novo synthesis is taking place it is concluded that phospholipid phosphokinase reactions at the platelet membrane are activated with thrombin aggregation. Accordingly, phosphoinositide kinases have been demonstrated in isolated platelet membranes.(Supported by the Deutsche Forschungsgemeinschaft.)
The Effect of a Platelet Inhibiting Drug (Sulfinpyrazone) in the Therapy of Patients with Transient Ischemic Attacks (Tia’s) and Minor Strokes
Authors: Robertson J. T. , Dugdale M. , Salky N. , Robinson H. 
Published: June 2019

A prospective double blind randomized trial of sulfinpyrazone and placebo is described in patients with TIA’S and minor strokes. The criteria for entry into the Study were patients with at least two transient ischemic attacks within a two-week period or patients with a minor fixed neurological deficit resulting from cerebrovascular occlusive disease. All patients had routine laboratory, special platelet aggregation studies, and cerebral arteriography. Several had initial and subsequent platelet survival studies. To insure equivalence of the two groups, patients were randomly assigned to categories reflecting their risk factors and age. Patients were followed every three months with appropriate laboratory and platelet studies. Interval follow-up occured when side effects or additional symptoms appeared.When patients failed on sulfinpyrazone, they were placed on sulfinpyrazone and Coumadin. Patients who failed on placebo were placed on sulfinpyrazone followed by sulfinpyrazone and Coumadin if subsequent failure occured. Failure was defined as two transient ischemic attacks within a two-week period or an additional stroke syndrome.New patients will be enrolled for three years, and all patients will be followed for five years. All data is incorporated into computer files.Preliminary results relating to the first sixty patients will be presented.
The Role of Heparin on the Inhibition of Platelet Adhesion to Damaged Arterial Endothelial Surface
Authors: Essien E. M. , Kinlough-Rathbone R. , Moore S. , Mustard J. Fraser 
Published: June 2019

A technique for the isolation of rabbit thoracic aorta in a form in which it could withstand normal pressure in an in vitro system was developed. Selected segments of the aortae from different animals were damaged mechanically. These were then flushed through rapidly with a suitable dilution of heparin from hog mucosa and the excess heparin was washed off. When such treated aortae were exposed to rabbit platelets, adhesion of platelets to such surfaces compared to non-heparinised ones was significantly depressed (P < 0.001). A similar effect was demonstrable on undamaged aortic surfaces (P < 0.006).It is suggested that heparin may interact directly and rapidly with damaged vascular surfaces and inhibit platelet adhesion to them. The significance of these results with particular reference to therapeutic concepts is discussed.
Rabbit Subendothelium - Human Platelet Interaction, a New Tool for Pathogenesis of Long Bleeding Time
Authors: Michel H. , Bodevin E. , Caen J. P. 
Published: June 2019

Interaction of human platelets with previously denuded rabbit aorta provides a new tool for the estimation of platelet function in inherited and acquired platelet disorders. The interaction with the sub endothelium was estimated morphometrically by the Baumgartner technique.It is already known that in the Bernard-Soulier syndrome, adhesion-aggregation to purified collagen and platelet aggregation in the presence of all the inducers acting through ADP are normal. In contrast bovine factor VIII and ristocetin do not aggregate the Bernard-Soulier platelets which adhere to subendothelium at only approximately 10 percent of the normal range.In thrombasthenia, adhesion to collagen is normal but primary or secondary ADP-induced aggregation is absent. Adhesion to rabbit subendothelium is reduced by 50 percent but always a monolayer of cells was seen.In a 65 year old patient who has an acquired haemorrhagic disorder with a long bleeding time and a normal platelet count her isolated platelets do not respond to ristocetin while they aggregate normally with collagen and ADP. Adhesion of her platelets to subendothelium is reduced by 50 per cent.It is therefore postulated that rabbit subendothelium-human platelet interaction provides a method for a better understanding of pathogenesis of long bleeding time.
Delayed Adhesion to Subendothelium and Defective Aggregation of Platelets from Rats with Storage Pool Disease (SPD)
Authors: Tschopp Th. B. , Baumgartner H. R. 
Published: June 2019

The inherited hemorrhagic diathesis in the Fawn-hooded rat has been shown to closely resemble the SPD in human patients. To study platelet interaction with surfaces, pooled citrated rat blood was circulated for periods of 2.5, 5 or 10 min through a perfusion chamber containing 2 everted segments of rabbit aorta previously denuded of endothelium. One segment was untreated, the second digested with a-chymotrypsin which removes amorphous material and microfibrils, and thus exposes elastin and islands of collagen fibrils. After perfusion, platelet-surface interaction was evaluated by a morphometric technique. On subendothelium exposed to blood of control rats, platelet adhesion amounted to 61%, 85% and 82% after 2.5, 5 or 10 min respectively. Significantly diminished adhesion (31% and 47%) with blood of SPD rats after 2.5 and 5 min became unsignificant (60%) after a 10 min perfusion period. This delayed adhesion was paralleled by an inhibition of SPD rat platelets to spread out on subendothelium as indicated by an increased ratio of contact/spread platelets of 1.4 compared with 0.2 found in controls after perfusion for 2.5 min. Platelet adhesion was unaltered on digested segments. Platelet thrombus formation (aggregation) observed with control blood was small (< 5%) and transient on sub-endothelium. On digested subendothelium however, platelet thrombi covered 50% of the surface after 10 min exposure. In contrast, virtually no platelet thrombi were observed with blood of SPD rats on either surface.Inhibition of spreading by an unknown, probably membrane associated defect explains the delayed platelet adhesion reaction observed with blood of SPD rats. The strong inhibition of platelet accumulation is probably due to diminished storage pool adenine-nucleotides and thus to a defective release reaction during spreading.
Anticoagulant Prophylaxis in Chronic Haemodialysis
Authors: Remde W. , Funke K. 
Published: June 2019

In 15 patients with chronic uraemic syndrome anticoagulant prophylaxis was carried out with chloride phenindione during three to twelve months. Indications were: repeated clotting of the Scribner shunt, unfavourable localisation of the shunt or difficulties during the implantation which let expect a shunt clotting.In spite of the heparinisation during the haemodialysis we succeeded in maintaining the Quick level between 15 and 35 percent. In all cases the incidence of shunt clotting was considerably reduced. Severe bleeding complications did not occur.
Heparin Therapy Monitoring Tests – Effects of Method and Patient Variables upon Accuracy
Authors: Mink I. B. , Fitzpatrick J. E. 
Published: June 2019

Tests utilizing the recalcification time of whole blood or plasma (e.g. A. P. T. T.) to monitor heparin therapy of a patient with malignancy and an accompanying thrombotic disorder, are subject to unpredictable in-vitro changes which occur during the time interval between withdrawal of blood from the patient and eventual testing in the laboratory. Significant reduction or prolongation of clotting time occurs in as little as five minutes, necessitating the performance of the test (whole blood recalcification or alternately centrifrigation and plasma recalcification) as rapidly as possible after patient contact.Correlations are presented between the direction and magnitude of these time-related changes and methodology variables (venipuncture stress, tube surface, decalcifying agent, storage temperature) as well as patient variables (heparin dosage, PF-4 activity, clotting factor lability, heparin tolerance). Repeated testing of the same blood samples may provide a, pattern of change which reflects in-vivo heparin catabolism.
The Significance of Prothrombin Assay Method Using Echis Carinatus Venom in Disseminated Intravascular Coagulation Syndrome
Authors: Sakuragawa N. , Takahashi K. , Matsuoka M. 
Published: June 2019

Prothrombin is decreased in disseminated intravascular coagulation syndrome (DIC). Prothrombin is estimated by the assay method using echis carinatus venom: 0.1 ml of 0.1% fibrinogen solution, 0.1 ml of one to ten diluted specimen and 0.1 ml of echis carinatus venom solution (0.01 mg/ml) are mixed in the test tube at 37° 0, and checked clotting time. From the standard calibration curve, prothrombin is shown by percentage in a normal person.Prothrombin activity by the regular assay method using tissue thromboplastin is lower than the assay method using echis carinatus venom in DIC.Thrombin which is produced in the blood of DIC splits prothrombin molecule to prethrombin. Prothrombin cannot be assayed by using tissue thromboplastin, but assayed rather by echis carinatus venom. This fact is proven from the results of SDS-dise electropboresis”pattern of purified prothrombin activated by thrombin or echis carinatus venom, by animal studies of DIC rabbit infused with thrombin, and by examination of DIC blood.‘ The assay method using echis carinatus venom is concluded to be useful to diagnose DIC.