bluuebunny/crossref_metadata_2025_split huggingface dataset:
Isolation of the Antithrombin-Thrombin Complex and Platelet Factor 4 by Solid Phase Heparin
Authors: Bleyland H. , Róka L. 
Published: May 2019

Solid-phase-heparin as heparin-agarose [Hep-Ag] was used for the isolation of the complex formed by antithrombin and thrombin. This complex has a lower affinity to heparin than antithrombin III. The complex has no antithrombin activity. The increase of the complex during blood coagulation can be seen by the two-dimensional Immunoelectrophoresis in agaroee, which contains heparin (Sas et al., Thromb.Res. 6, 87-91, 1975).Platelet factor 4 (PF 4) was isolated by a three step procedure: 1. precipitation by divalent cations according to Burstein, 2. adsorption to Hep-Ag and desorption with high salt concentrations, 3. desalting over Sephadex G 25 fine. PF 4 was prepared from isolated platelets, platelet rich plasma and serum.
A Tentative Cause of Discrepancy Between FVIII:C Estimation
Authors: Seghatchian M.J. 
Published: May 2019

Biochemical analysis based on the molecular size and change was performed on normal, patient plasmas and clinical concentrate to differentiate various molecular forms of FVIII:C. Assay of the effluent fractions by one stage, two stage and chromogenic methods revealed two major peaks of activities, measured to differing extents by various methods. Thromboplastin generation methods (two stage clotting and chromogenic) were particularly sensitive to smaller forms, which had a faster electrophoresis mobility and eluted in the gamma globulin region. The one stage method measured mainly the aggregated forms (MW> 300.000), with the slower electrophoretic mobility.A discrepancy of about 30% between the two methods could account for the detection of the smaller form, which predominated in plasma rather than concentrate. This had a preferential adsorption on Al(OH)3 and some FVIII.C neutralising activity. A similar peak of activity was identified in haemophilia and V.Wd. plasma isolated on sepharose suggesting that the whole plasma contained an inhibitory factor acting on the clotting activity. Excess factor X and traces or thrombin-like enzymes could be identified in this region. Thus the role of these factors in accelerating the rate of FXa generation by activating FVIII can not be excluded.Regardless of the molecular nature of this form of FVIII, this activity may play an important role in controlling haemstasis via VIII activation and may explain the discrepancy between assay of plasma versus concentrate.
Altered Platelet Factor X Activating Activity in Myeloproliferative Disorders
Authors: Cortellazzo S. , Colucci M. , Barbui T. , Semeraro N. 
Published: May 2019

The pathogenesis of the haemostatic disorders in patients with myeloproliferative diseases has not yet been completely elucidated. Several platelet function abnormalities have been reported but they do not always correlate with the clinical manifestations. In this report a recently described platelet coagulant activity (factor X activating activity) was studied in 2 patients with essential thrombocythacmia, 10 with polycythaemia vera, 4 with chronic myeloid leukaemia and 2 with reactive thrombocytosis. It was significantly reduced in the 5 patients with bleeding tendency, and was also reduced in one patient with a history of peripheral ischaemia and in 3 patients with no haemostatic complications. It was either normal or increased in the remaining patients who had no haemostatic complications. In the two subjects with lowest activity (5 and 131) and most serious bleeding, chemotherapy resulted in normalisation of the platelet count and of platelet coagulant activity and in disappearance of the bleeding episodes. Our results suggest an association between bleeding tendency and reduced platelet coagulant activity. These findings may be of relevance to 1) the pathogenesis of abnormal bleeding in patients with myeloproliferative disorders and 2) the understanding of the role of platelet coagulant activities otter than pLatelet factor 3 in disturbed haemostasis.Supported by CNR (Italy).
Regular Haemodialysis Therapy (RDT) Induces A Prothrombotic State
Authors: Turney J. , Woods H.F. , Weston M.J. 
Published: May 2019

To determine whether activation of coagulation factors and platelets, reported during haemodialysis results in a prothrombotic state we have studied indices of coagulability in 15 undialysed and 32 dialysed uraemic patients. Mean plasma fibrinogen (g/1) in uraemic patients (3.53) was significantly higher than in controls (2.45) and rose further in dialysed patients (3.81). Factor VIII coagulant activity (CA) was greater in dialysed (202 ± 15.9%) than in undialysed uraemic patients (184 ± 14.2%) both being significantly greater than control (84 ± 3.9). Similarly Factor VIII related antigen (RA) was higher in dialysed patients (216 ± 18.5%) than uraemics (156 ± 9.6%) (control = 94 ± 5.6%). The mean RA/CA ratio and the frequency of a high RA/CA ratio (< 1.5), an index of thrombin induced consumption of Factor VIII-CA and intravascular coagulation, were higher in dialysed than nondialysed patients.Despite the higher circulating levels of procoagulants and the evidence of thrombin activation the availability of heparin cofactor-antithrombin III (AT III) was lower in dialysed (154%) than in uraemic patients (159%) though in both groups AT III levels were higher than in controls (100%).These results indicate that RDT is associated with a prothrombotic state which is not completely compensated for by an increase in antithrombin III.
Anti-A Content of Intermediate-Purity Concentrates of Factor VIII
Authors: Smith J.K. , Bowell P.J. , Gunson H.H. , Snape T.J. 
Published: May 2019

Haemolysis may be induced in haemophiliacs of blood group A if they receive very large doses of concentrates containing high levels of anti-A. The anti-A content of factor VIII concentrates made at PFL has been, measured by an automated haemagglutination method. The standard was a pool of 500 sera of random blood groups, assigned a value of 100 units per ml. 23 batches of concentrate prepared from 5 1 packs of FFP, each containing about 24 donations of random blood groups, contained 23.7 ± 4.1 (mean ± S.D.) units anti-A/iu factor VIII.It was predicted that, if 5 l pools were replaced by single donations of FFP which were not mixed until thawing and collection of the cryoprecipitate, there would be less neutralisation of anti-A by group A donations and the anti-A level in the concentrate would be increased. Unexpectedly, the anti-A content of 9 batches prepared from single donations of random blood groups was 5.8 ± 1.5 units/iu factor VIII, significantly lower than for batches made from 5 1 packs. It is postulated that free anti-A is less susceptible to cryoprecipitation than is anti-A completed with A substance during pooling of group O and A plasmas at 20°. After re-solution of the cryoprecipitated complex, equilibrium may be re-established to give free anti-A.
Sequential Platelet and Fibrinogen Turnover Studies Associated with left Ventricular Assist Device (LVAD) Implantation
Authors: Rodvien R. , Dalal K.B. , Mitchell R. , Litwak P. , Bosak J. , Baleix J. , Hill J.D. 
Published: May 2019

Quantitation of thromboembolism is necessary to guide polymer fabrication and anticoagulant use for artificial organ implantation. Therefore as part of the LVAD program we have solid-phase radioiodinated bovine fibrinogen and developed an autologous 111In technique to quantitate platelet survival. Mean platelet survival time(n/a) by the method of Murphy and Francis was 130±20 hrs for 10 animals; platelet aggregation and serotonin release were unaffected by the labelling procedure, n/a for homologous fibrinogen was 55.0±7.3 hrs. for 11 cows; clottability was 93%.LVAD implantation of the Thoratec Model VIC devices with textured surfaces produced both shortened platelet (47+4.4 hrs.) and fibrinogen survival (30±4.6 hrs.) at 24 hrs. despite coumadin, aspirin and persantin. Survival curves changed from linear to curvilinear, suggesting consumption. Sequential studies at 1, 2 and 4 weeks showed continued platelet and fibrinogen consumption though to lesser degrees than at 24 hrs. Despite coumadin, aspirin and persantin, on-going consumption is occurring and can be quantitated, thereby providing a laboratory monitor to guide future development and clinical use of the LVAD.
Attempted Determination of Endogenous Heparin in Blood
Authors: Jacobsson K.-G. , Lindahl U. 
Published: May 2019

A method was developed for the micro-scale determination of heparin in blood plasma. After extraction with water-saturated phenol glycosaminoglycans were recovered from the aqueous phase by ion-exchange chromatography on DEAE-cellulose. The heparin content of the product was determined by a colorimetric antithrombin-activation assay. Recoveries of 40-60% of both radioactivity and biological activity were obtained when the method was applied to the reisolation of 3H-labeled heparin, added at a concentration of 20 ng (about 0,003 unit) per ml blood. In the absence of exogenous heparin no antithrombin-activating material could be detected. The amount of endogenous heparin, if any, in human blood was calculated to less than 2 ng (about 0.0003 unit) per ml.(Supported by grant No. 2309 from the Swedish Medical Research Council)
On the Release Function of Adhering Platelets
Authors: Malmgren R. , Larsson R. , Olsson P. , Tornling G. , Unge G. 
Published: May 2019

A Method for measuring the continuous uptake and release of serotonin during 60 minutes by platelets adhering to a polymer surface is presented.Heparinised human blood with autologous 51Cr and 14C-serotonin labelled platelets is exposed to the polymer in Chandler loops rotated slowly for different periods. Initially the adhering platelets take up serotonin from non-adhering aggregating platelets by an active process and then slowly begin to release serotonin. Acetylsalicylic acid treated platelets adhere and take up serotonin to the same extent as untreated platelets, but do not undergo a release reaction.Coating of the polymer surface with fibrinogen prior to blood exposure or with fibrin (achieved by thrombin treatment of the fibrarinogen adsorbate) does not affect the degree of adhesion and serotonin uptake, but inhibits the release reaction. When only fibrino-peptide A is split off with Defibrase from the fibrinogen layer the release function of the adhering platelets reappears.It is concluded that the release mechanism of adhering platelets is not only dependent of the functional state of the platelet itself, but also on the ultimate composition of the protein layer to which the platelets adhere.
Effects of Aspirin and Sulfinpyrazone on Thromboxane and Prostacyclin Synthesis in Rabbits
Authors: McDonald J.W.D. , Cerskus A.L. , Ali M. 
Published: May 2019

Arachidonic acid (AA) or collagen were infused into rabbits causing intravascular platelet aggregation with thrombocytopenia, hypotension and death. Thromboxane and prostacyclin synthesis were measured by radioimmunoassay of plasma TXB2 and 6-keto-PCF1α. The effects of pretreatment with aspirin (ASA) or sulfinpyrazone (SPZ) were assessed.Death in drug-treated rabbits was always associated with elevations of plasma TXB2 (1-40 ng/ml) and of 6-keto-PGF1α (1-20 ng/ml). Collagen produced only small elevations of plasma TXB2 compared to AA but protection by ASA correlated better with inhibition of TXB2 and 6-keto-PGF1α synthesis than with inhibition of aggregation. Low dose ASA produced less inhibition of prostacyclin synthesis than high dose ASA but was less effective in preventing thromboxane synthesis and death.
Red Cell Filterability and Cardiovascular Risk Factors
Authors: Lagrue G. , Marcel G. A. , Faucher G. , Grumel J.M. , Beiler D. , Branellec A. 
Published: May 2019

Red cell deformability, which allows cells of 7 μ diameter to flow through capillaries not larger than 3 μ, can be approached by the measure of blood filterability on Nuclepore 5 u filters (Reid H.L. et al. J. Clin. Pathol. 1976; 29: 855). Filterability seems reduced in certain states predisposing to thrombosis.We have, in 72 patients, correlated red cell filterability (using two batches of filters) expressed in μl/s, with the number of cardiovascular risk factors present (high blood pressure, overweight, diabetes, hyperuricemia, hyperlipemia, smoking). Statistical analysis has been performed using regression analysis for each batch of filters, and both significance levels have been combined using Fisher’s method. The table illustrates the relationship between the number of risk factors and filterability. There is a statistical difference between groups as a whole (p<0.0l). The difference is highly significant between 0 and 4 risk factors (P<0.0005). Filterability decrease is also directly correlated with the number of cigarettes smoked per day (p<0.05). This is significant innen (p<0.05), but not in women.
Plasminogen Activator and Factor VIII in Cirrhosis Following Infusion of Lysine Vasopressin and Triglycyl Lysine Vasopressin
Authors: Prowse C.V. , Douglas J.G. , Cash J.D. 
Published: May 2019

While lysine vasopressin (LVP) has been used for many years for the treatment of cirrhotic patients with bleeding oesophageal varices, on the basis of its ability to cause splanchnic vasoconstriction, its use remains contraversial. Previous studies have shown that infusion of this drug to normal subjects results in a rapid increase in plasminogen activator and factor VIII. When infused into cirrhotic patients with varices we found that LVP caused a large increase in the, already raised, level of plasminogen activator (and factor VIII). This increase in fibrinolytic potential might contribute to poor deposition of fibrin in bleeding patients. .In contrast infusion of the analogue triglycyl lysine vasopressin (GVP) in the same patients produced no change in plasminogen activator or factor VIII. GVP retains the vasoconstrictive properties of LVP and has a considerably longer half-life. In view of these advantages clinical trials of the use of GVP in gastrointestinal bleeding are warranted.
Small Doses of Subcutaneous Heparin, Plasma Free-Fatty-Acids, and the Incidence of Ventricular Arrhythmias in Patients with Acute Myocardial Infarction
Authors: Arnesen H. , Skjæggestad Ø. , Wik N. 
Published: May 2019

The frequency of deep vein thrombosis (DVT) diagnosed with the 125I-fibrinogen technique in patients with acute myocardial infarction (AMI) has been found to be reduced frcm about 20% without anticoagulation to about 5% with warfarin or small doses of subcutaneous heparin.A somewhat higher incidence of ventricular tachycardia in patients with AMI treated with small doses of subcutaneous heparin has been reported. A possible mechanism might be heparin-induced activation of lipoprotein lipase with consequent increase of plasma free-fatty-acids (FFA), which have been found to be arrhythmogenic in patients with AMI.In the present prospective trial, 99 patients with AMI and a history of less than 12 hours were allocated at random to treatment with subcutaneous heparin 5000 IU twice daily, or warfarin. In a randomized subsample of 21 patients fasting FFA analyses were performed before and 2 hours after the administration of anticoagulants on day 1 and 2.No measurable increase in FFA concentrations was demonstrated in the heparin-treated patients, in spite of a significant influence on the thrombin clotting time.The frequency of ventricular arrhythmias as detected by continous tape recordings was equal in the two treatment groups.It is concluded that subcutaneous heparin 5 000 IU every 12 hours seems to be a safe measures of prophylaxis against venous thromboembolic ccmplications in patients with AMI.
Prevention of Venous Thromboembolism
Authors: Salzman E.W. 
Published: May 2019

Prospective clinical trials have shown that reduction in frequency of deep vein thrombosis (DVT) and pulmonary embolism (PE) can be achieved by physical preventive methods or by administration of antithrombotic drugs. There is however confusion concerning the best form of prophylaxis for different patient groups, difficulty in translating results of clinical trials directly into practice, and ignorance of the dollar cost of the various regimes. Critical analysis of the literature permits prediction of expected frequencies of fatal PE and of DVT and complications of therapy, but questions remain. The prevalence of silent PE in different populations is not established. Definition of a high risk group is imprecise, so patients at lesser risk are exposed to the side effects of antithrombotic prophylaxis with little to gain. Since the natural history of DVT is poorly understood, side effects of anticoagulant therapy are also inflicted on many with little likelihood of PE for the benefit of a few susceptible patients. Apparent differences in rate of occurrance of DVT on the two sides of the Atlantic are suggested but unproven and not explained.Despite these uncertainties, determination of cost/effectiveness of preventive programs is possible and can provide a workable guide to clinical practice.
Effect of PGI2 and Its Derivatives on Platelet Adherence Aggregation and PF3 Availability
Authors: Fésüs L. , Stadler I. , Hársfalvi J. , Balogh M. , Kovács E. , Muszbek L. 
Published: May 2019

10-8M PGI2-Na completely inhibited collagen induced aggregation of human platelets and the concomitant appearance of platelet factor 3 activity, but did not affect the adherence of platelets to collagen fibrils. At the same time, the presence of PGI2-Na could prevent the retention of platelets by glass beads.Comparing to the inhibition of ADP induced aggregation a higher dose of PGI2-Na was needed to inhibit platelet aggregation by ionophore A23187. Furthermore, unlike ADP aggregation, increasing dose of ionophore could counteract the inhibitory effect of PGI2-Na. The shift of platelet actin from G to F from during ionophore aggregation could be prevented by appropriate dose of PGI2-Na. PGI2 derivatives (Chinoin, Hungary) with increased stability, although in higher doses, exerted activities similar to PGI2-Na.
Lipid Composition and Lipid Synthesis in Guinea Pig Megakaryocytes and Platelets
Authors: Schick E.P. , Schick P.K. 
Published: May 2019

Lipid composition and lipid synthesis have been compared in guinea pig megakaryocytes and platelets. Megakaryocytes were isolated from guinea pigs to 85% purity. Lipids were extracted and were separated by thin layer chromatography. Phospholipid (PL) content was determined by measurement of lipid phosphorus, and cholesterol and fatty acids were quantitated by gas-liquid chromatography. PL composition of megakaryocytes was:PS + PI 15.2%; SM 14.0%; PC 40.1%; PE 30. 6%. PL composition of platelets was: PS 10.1%; PI 4.5%; SM 16.5%; PC 39.5%; PE 29.6%. The cholesterol:PL ratio was 0.35 for megakaryocytes and 0.55 for platelets. The major fatty acids in the PL were: (% of total)Megakaryocytes and platelets were incubated for 1.5 hr with 14C-acetate. Megakaryocytes incorporated acetate into cholesterol and other sterols, ceramide, and PL (0.060, 0.016 and 0.012 nmoles/105 cells). Platelets incorporated acetate into ceramide and PL (0.02 and 0.06 nmoles/109 cells) but only trace amounts into sterols. There appears to be active biosynthesis of cholesterol in megakaryocytes but not in platelets.
The Detection and Importance of Intravascular Platelet Aggregation in Surgical Shock
Authors: McCollum C.N. 
Published: May 2019

Intravascular platelet aggregates (IPA) have as yet avoided detection in shocked patients hence their role in the aetiology of “shock lung” remains controversial. Screen filtration pressure (SFP) has only been shown to measure aggregates in vitro.A modified screen filtration technique was evaluated in 43 surgical patients. The characteristics (height,slope) of the pressure wave were compared with the number of aggregates seen to occlude filter pores on scanning electron microscopy (SEM). In 80 estimations on femoral vein blood the slope of the SFP curve was utilised improving SFP/ SEM correlation to r= .93. These aggregates arise in vivo as they were rarely detected in blood from the arm and IPA levels in femoral blood were not influenced by EDTA priming of the syringe. In 36 preoperative estimations mean SFP slope was identical to that in 14 patients after minor surgery (1.5 ± SD 1.6). After major surgery in 29 patients this value was elevated at 7.1 ± 6.1 (P<.001). Seventeen of these patients with SFP slope greater than 5 suffered a mean fall in arterial P2 at 5 days post operation of 1.85 KPa (13.9 mm Hg) which was significantly greater than that in the other major cases (0.85 KPa, 6.4 mm Hg)(P <.05). SFP also correlated closely with the fall in platelet count on day 1 post operation (r= .82, P< .001).Intravascular platelet aggregates arise in the veins of the lower limb immediately after major surgery. They can be measured by the screen filtration technique described and may be related to pulmonary dysfunction.
Blood Contact Properties of Surfaces Coated with Sulphate Groups and Different Glucoseaminoglycans.
Authors: Larsson R. , Busch C. , Eriksson J-C. , Lagergren H. , Lindahl U. , Olsson P. 
Published: May 2019

Quantitative measurements of platelet adhesion and activation of plasma coagultlon were performed on polyethylene (PE) and PE-modified by sulphation and by adsorption of colloidal particles containing heparin, dermatan- and heparan sulphate.Tubings with the different surfaces were inserted as arteriovenous shunts in acute experiments on dogs with 51Cr-labelled platelets. On all the modified PE surfaces the platelet adhesion was minimal in comparison with the unmodified PE. Only the heparinized surface could prevent activation as measured by radioimmunmoassay of fibrinopeptide A.It is concluded that surface-located sulphate groups make a surface platelet-compatible, but not necessarily non-thrombogenic. For complete non-thrombogenicity other structures in the heparin molecules than sulphate groups appear Important.
Absence of the Complete Platelet-Specific Alloantigens Zw (PlA) On Platelets in Glanzmann’S Thrombasthenia and the Effect of Anti-Zwa Antibody on Platelet-Function
Authors: von Leeuwen E.F. , Zonneveld G.T.E. , von Riesz L.E. , Jenkins C.S.P , van Mourik J.A. , van dem Borne A.E.G.Kr. 
Published: May 2019

The expression of the platelet-speciftc alloantigens on the platelets from 6 patients with Glanzmann’s Thrombasthenia (G.T.) and their nearest relatives was studied. The alloantigens Zwa (PIAl) and Zwb(PIA2) were found to be completely absent from thrombasthenic platelets while the alloantigens of the Ko-system were found to be normally expressed. The alloantigen Baka(phenotypefrequency 90.2%) was absent on the platelets from 4 studied G.T. patients. The platelets of all the family members reacted positively with anti-Zwa, negatively with antt-Zwb serum. SDS-PA gel electrophoresis of G.T. platelet membranes demonstrated a marked deficiency of the glycoproteins IIb and IIIa. Glycoprotein analysis of the platelet membranes from the family members of 3 of the 6 patients reveoled no apparent abnormalities.Pre-incubation with anti-Zwa containing plasma strongly inhibits ADP-and collagen induced aggregation of platelets from normal Zwa homozygous individuols with a slight inhibition of the aggregation induced by ristocetin. Zwa antibodies did not affect the functions of platelets from ZWb homozygous individuals. Thus binding of Zwa antibodies induces a thrombosthenis-like state.