bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sustained Lymphatic Delivery of Fibrinogen after Induced Afibrinogenemia
Authors: Young Margaret C. , Kolmen S. N 
Published: June 2018

SummaryLymphatic fibrinogen levels were maintained for a long period in the absence of plasma fibrinogen. Although a portion of the additional fibrinogen required may have been the result of de novo synthesis, an additional source, that of previously sequestered fibrinogen in storage sites, must have been present.The amount of fibrinogenolysis induced, although complete in the plasma compartment of dogs, was not as effective in the lymphatic compartment. One resultant of fibrinogenolytic induction in vivo was retardation of fibrin polymerization in incubated lymph samples.
Clotting Factors and Fibrinogen Split Products in the Extravascular Space
Authors: Benz J. J 
Published: June 2018

SummaryFactors I, II, V, VII-complex, X, fibrinogen-split products and fibrinolysis were assayed in 42 transsudates, 69 exsudates and simultaneously in the blood of the respective patients.The vitamin K dependent factors II, VII-complex and X were present in all extravascular specimens; factors V and clottable fibrinogen only in the majority of exsudates and the minority of transsudates. Fibrinogen-split products were found in most specimens even though the simultaneously tested serum of the respective patients was free of them. The collected quantitative data indicate that all clotting factors enter the extravascular space in direct proportion to their concentration in plasma and to the protein content of the extravascular fluid. Local extravascular lysis accounts for the low values of clottable fibrinogen and factor V and for the presence of fibrinogen split products. It is possible that the physiologic catabolism of these factors is mainly extravascular.
The Modification of Experimental Occlusive Arterial Thrombosis in the Rat by Malayan Pit Viper Venom
Authors: Chan K. E 
Published: June 2018

SummaryThe effect of Malayan pit viper (Ancistrodon rhodostoma) venom on the fate of experimental arterial thrombosis was studied in rats. A suitable daily dose of venom (500 μg) was used to induce hypofibrinogenaemia in the treated rats for the greater part of each of three consecutive post-operative days.The treated animals showed a statistically significant overall reduction in the incidence of both red thrombus formation and thrombotic arterial occlusion when compared to a control group. This antithrombotic effect of the venom could be observed in the 7-day period following the cessation of the treatment.
Prothrombin Purification by Chromatography
Authors: Landaburu R. H , Albado Emilia , Santillán R 
Published: June 2018

SummaryBovine prothrombin with specific activity above 40,000 u/mg of tyrosine may be obtained by chromatography on Amberlite AG3-X4. The product does not yield autoprothrombin C in appreciable amounts. A fraction separated by this procedure behaves as a procoagulant when replaced into the purified prothrombin.
Metabolic Studies of Vitamin K1-14C and Menadione-14C in the Normal and Hepatectomized Rats
Authors: Losito R , Owen C. A , Flock E. V ,   Rochester, Minnesota
Published: June 2018

SummaryThe metabolism of vitamin K1-
14C and menadione-14C (vitamin K3-14C) was studied in normal and hepateetomized rats. After the administration of menadione, about 70% of the 14C was excreted in the urine in 24 hrs in both types of rats. Two urinary metabolites were identified by enzymatic hydrolysis: one a glucuronide and the other a sulfate of reduced menadione. Thus, the liver is not necessary for the metabolism of menadione. In the vitamin K1 studies, the intact rats excreted only 10% of the 14C and the hepatectomized rats excreted less than 0.5%. The retention of vitamin K1 may explain its superiority over menadione as an antidote for overdosages of oral anticoagulants.
Properties of 3-(1-Phenyl-Propyl)-4-Oxycoumarin (Marcoumar®) in the Plasma when Tested in Normal Cases and under the Influence of Drugs
Authors: Seiler K , Duckert F 
Published: June 2018

SummaryA fluorimetric method served to determine Marcoumar in blood plasma. The biological half-time of Marcoumar after an administration of 2.2 mg/10 kg is 6½ days. Variations in maintenance dose requirements seem not to be primarly determined by differences in absorption or excretion of the anticoagulant drug. In therapeutical concentrations about 99% of the drug are bound to plasma protein. Marcoumar can be displaced in vitro from plasma protein by different drugs. The anticoagulant effect is not increased in every case in which the anticoagulant is displaced in plasma from its protein binding.
Studies on Thrombolysis with Streptokinase
Authors: Gottlob R , Blümel G , Piza F , Brücke P , Böhmig H. J 
Published: June 2018

Summary1. Human thrombi of various ages obtained by surgery were incubated in SK solution. Whereas thrombi up to 2 days old showed no considerable lysis, older thrombi, in some cases more than 1 month old, showed good lysibility in SK.2. The good lysibility of older thrombi was reproduced in in vitro whole blood clots.3. Similar to the findings obtained in experimental thrombi, we found that in in vitro whole blood clots retraction goes along with a marked decrease in the water content, whereas we find again a moderate rise with increasing age.4. If we add 131I-labelled human serum albumin to the supernatant of in-vitro clots, we see an increased absorption of albumin, particularly in the second and third day after clotting.5. Massive hemolysis sets in on the second and third day in whole blood clots incubated at 37 centigrades in their own serum.6. The following are discussed as possible causes for the improved lysibility of older thrombi and clots : renewed absorption of plasminogen from the milieu ; the release of ferments that may be activated by SK in the process of cytolysis, and a decrease in the content of plasmin inhibitors.7. Based on the findings the suggestion is advanced to attempt lytic therapy with SK even in the case of older clinical thrombi.
Release of Platelet Factor 4 in Vivo during Intravascular Coagulation and in Thrombotic States
Authors: Farbiszewski R , Niewiarowski S , Worowski K , Lipiński B 
Published: June 2018

SummaryPlatelet factor 4 released from platelets into the circulating blood was determined using both the heparin thrombin time and paracoagulation methods. It has been found that thrombin injected intravenously into rabbits releases large amounts of this factor. Infusion of plasmin does not release this factor and this finding may be of importance for the differential diagnosis between disseminated intravascular clotting and primary fibrinolysis. PF4 is not released during the hyper coagulable condition induced by HgCl2 intoxication. Only small amounts of this factor are released after contact factor infusion.A significant elevation of extraplatelet PF4 was found in 23 patients with fresh coronary thrombosis and in 9 patients with thrombophlebitis and thromboembolic complications.The significance of the above findings for the pathogenesis, treatment and laboratory diagnosis of thrombotic diseases with particular reference to heparin tolerance test is discussed.
Différents états moléculaires du facteur II (prothrombine). Leur étude à l’aide de la staphylocoagulase et d’anticorps anti-facteur II
Authors: Soulier J. P , Hallé Liliane , Prou-Wartelle Odette 
Published: June 2018

RésuméNous avons examiné dans quelles conditions des préparations de facteur II humain, plus ou moins purifiées, se dissocient en présence de 25 p. cent de citrate de soude ou de sulfate d’ammonium 2 M. L’addition de thrombine intervient en neutralisant l’anti-thrombine contaminant certaines fractions et en apportant du facteur X.Nous avons mis en évidence au cours de l’incubation une dissociation entre l’activité prothrombine (capacité de former de la biothrombine avec les activateurs physiologiques) qui décroît et l’activité prothrombine-coagulase (capacité de former de la thrombine-coagulase en présence de staphylocoagulase) qui s’accroît. Il est ainsi possible dans l’espèce humaine de suivre la dissociation du facteur II humain et d’apprécier à l’aide de staphylocoagulase la formation d’un produit intermédiaire décrit par Seegers et désigné récemment par cet auteur du nom de préthrombine. La mesure de l’activité prothrombine-coagulase n’est pas modifiée par l’addition d’hiru-dine qui neutralise la thrombine éventuellement formée au cours de l’ auto-activation.Si la staphylocoagulase est inactive à l’égard du facteur II bovin, elle forme par contre avec le facteur II humain un complexe doué d’une activité thrombique (thrombine-coagulase). Ce complexe se forme plus vite lorsque le facteur II est dissocié au préalable en citrate de soude ou sulfate d’ammonium, c’est-à-dire que la « préthrom-bine » peut être estimée, directement par la staphylocoagulase. L’activité prothrombine-coagulase se développe en quelques secondes et ne nécessite ni calcium ionisé ni aucun co-facteur alors que la préthrombine n’est transformée que beaucoup plus lentement par l’ auto-prothrombine C de Seegers (homologue du facteur X activé).
Influence of Vitamin K on Restoration of Prothrombin Complex Proteins and Fibrinogen in Plasma of Depleted Dogs
Authors: Dulock M. A , Kolmen S. N 
Published: June 2018

SummaryThe action of vitamin K1 on dogs with reduced plasma concentrations of prothrombin and fibrinogen was studied. Thirty-two dogs were divided into two groups; each received either warfarin or nothing 24 hrs prior to blood cross-exchange with an erythrocyte-serum preparation. After exchange, each group was subdivided into dogs receiving either vitamin K1 or saline. Blood and lymph samples were obtained before exchange, after exchange, and at subsequent 2 hr intervals for 6 hrs. Prothrombin times and fibrinogen were among the measurements made.The data presented support the concept that warfarin blocks synthesis at a late stage where incomplete or precursor prothrombin-complex proteins can be accumulated intracellularly. Vitamin K enables continuation of prothrombin synthesis and enhances the release of prothrombin and fibrinogen into the plasma and lymphatic compartments. Warfarin also affects vascular integrity as suggested by alterations in lymph flow and hematocrit.
Abnormality in the Aggregation of Blood Platelets in Various Morbid Conditions and the Influence of Prostaglandins upon this Abnormality
Authors: van Creveld S , Pascha C. N ,   With technical assistance from Miss L. KERKMEESTER and Mrs. C. J. McEwan-van DER HORST
Published: June 2018

SummaryIn two young patients (belonging to the same family) with von Willebrand’s disease, an anomaly of the function of the blood platelets was observed, viz. a normal rapid initial aggregation of the platelets after addition of ADP, which after a few minutes was followed by an extraordinarily rapid disaggregation. This anomaly has very recently been described as an isolated anomaly. The same anomalous aggregation could be demonstrated in plasma of the father of the two patients, but he did not have von Willebrand’s disease.Some other observations of abnormally rapid disaggregation with ADP, after a normal initial aggregation, observed by us in patients with various morbid conditions, are communicated.The remarkable inhibiting action of one of prostaglandins (PGE1), even in very small amounts upon the ADP induced platelet aggregation could be confirmed. PGE2 also in very small amounts, markedly increased the aggregation by ADP in the cases investigated by us and was able to normalize the anomalous aggregation. It had, however, no effect on the absence of platelet aggregation with ADP in Glanzmann’s thrombasthenia.
Genetic Aspects of Hemostasis
Authors: Quick A. J 
Published: June 2018

SummaryHereditary defects resulting in inadequate syntheses of fibrinogen, prothrombin, factors V, VII, VIII, IX and X are quantitatively transmitted, therefore all affected members of a family are identical genetically. The concentration of the clotting factor in the blood is determined by the balance of the rate of synthesis to the rate of consumption or turnover. The required concentrations of these clotting factors to maintain hemostasis are strikingly low but below a critical level, traumatic bleeding occurs. The bleeding time is normal, and capillary or mucous membrane bleeding such as spontaneous epistaxis is uncommon or even absent. These states are transmitted as either autosomal or sex-linked recessives.Hereditary purpuric bleeding states are usually attributable to abnormal platelet function, to a defect in the autonomic nervous system that maintains the tonus of the microcirculation, or to the telangiectatic state in which the abnormality resides either in the structure of the capillaries or the mesenchymal matrix in which the micro vessels are imbedded. The thrombopathies constitute a group with various types of hereditary transmission. The Minot-von Willebrand syndrome and telangiectasia are transmitted as autosomal dominants. In most affected subjects, the bleeding is mild and superficial, usually from mucous membranes such as nosebleeds. In many the bleeding tendency is almost subclinical. Traumatic bleeding such as intramuscular hemorrhage and hemarthrosis is absent. The bleeding time in the severe cases is prolonged but may be normal in the mild bleeder unless prolonged by the ingestion of a drug such as aspirin.The clinical severity in the hereditary bleeding diseases is determined by: (1) the functional capacity of the gene responsible for the synthesis of the specific hemostatic factor, (2) the superimposition of a secondary hemostatic defect either hereditary or acquired, and (3) environmental factors which per se do not affect hemostasis. Hemophilia serves as the illustration. No severe bleeding occurs in pure factor VIII deficiency until the concentration is below the range of 1 to 2% of normal. On superimposition, for instance of telangiectasia on a mild hemophilia, the clinical manifestations are markedly accentuated. The simultaneous occurrence of even very mild Minot-von Willebrand syndrome in the hemophiliac will intensify the bleeding tendency, especially after the ingestion of aspirin. Environmental factors illustrated by trauma such as mild contusions, which in the normal do not even cause a bruise, may bring about intramuscular hemorrhages and hemarthroses, and thereby sometimes initiate a bleeding cycle.
Fibrinolytic Activity of Human Veins in Arms and Legs
Authors: Pandolfi M , Robertson B , Isacson S , Marie Nilsson Inga 
Published: June 2018

SummaryA modification of the fibrin slide method of Todd permitting a semiquantitative estimation of the fibrinolytic activity in tissue sections is described. By means of this technique, the authors have studied the fibrinolytic activity of the great saphenous vein and of superficial veins of the arm and leg in patients suffering from varices and in normal subjects. It was found that:1. Fibrinolytic activity is localized, in these vessels, mainly to the vasa vasorum of the adventitia. The media is moderately active. Intimal cells are active only when detached.2. The great saphenous vein is more active above than below the knee.3. The veins of the arm are definitely more active than the veins of the leg.4. The activator of plasminogen demonstrated in the sections by the fibrin slide method is a fairly stable enzyme still active after exposure to 60° C and resistent to moderate variations of pH.
Observations on the Effect of Glass Beads on Platelet Aggregation and Its Relation to Platelet Stickiness
Authors: Morris C. D. W 
Published: June 2018

Summary1. The concept of glass bead induced reversible and irreversible platelet aggregation is presented.2. The effect of glass beads in plasma and whole blood was observed microscopically. The microscopic observations were supported by experimental evidence.3. It is shown that phosphoenol pyruvate (PEP) and pyruvate kinase (PK) are capable of completely preventing aggregation if given before glass bead contact. This indicates that adenosine diphosphate (ADP) is the major factor in stimulating aggregation.4. It is shown that the ADP is released in this system, from the platelets, and not from the red cells.5. Haematocrit changes between 20% and 60% do not affect the platelet stickiness.6. The concentration of ADP apparently determines whether the aggregates become irreversible or not.7. Siliconised glass beads do not prevent aggregation; on the contrary, they increase both the observed rate of formation of aggregates, and the measured platelet stickiness.8. Addition of PEP and PK after glass contact causes the reversible aggregates to disaggregate. However, merely leaving the blood to stand for at least 30 min after contact, produces the same effect. This allows the measurement of pure irreversible aggregation.9. The desirability of measuring the irreversible aggregation is discussed.
In Vitro Assay of Platelet Adhesiveness with Washed and Tanned Human Red Cells
Authors: Zbinden G , Tomlin S 
Published: June 2018

SummaryAn in vitro system is described in which adhesion of blood platelets to washed and tannic acid-treated red cells was assayed quantitatively by microscopic observation. ADP, epinephrine and TAME produced a reversible increase in platelet adhesiveness which was antagonized by AMP. With Evans blue, polyanetholsulfonate, phthalanilide NSC 38280, thrombin and heparin at concentrations above 1-4 u/ml the increase was irreversible. The ADP-induced increase in adhesiveness was inhibited by sodium citrate, EDTA, AMP, ATP and N-ethylmaleimide. EDTA, AMP and the SH-blocker N-ethylmaleimide also reduced spontaneous platelet adhesion to red cells. No significant effects were observed with adenosine, phenprocoumon, 5-HT, phthalanilide NSC 57155, various estrogens, progestogens and fatty acids, acetylsalicylic acid and similarly acting agents, hydroxylamine, glucose and KCN. The method may be useful for the screening of thrombogenic and antithrombotic properties of drugs.
Activation of Blood Clotting and Inhibition of Fibrinolysis in Acute Pancreatitis
Authors: Gabryelewicz A , Niewiarowski S 
Published: June 2018

SummaryThe following changes in patients and dogs with acute pancreatitis or pancreatic necrosis were observed: shortening the plastic and glass clotting time, decrease of factor V, transistory decrease of fibrinogen followed by an increase of this factor, inhibition of euglobulin fibrinolysis, increase of plasminogen and antiplasmin.Autopsy examinations revealed many thrombi in pancreas and in other organs in dogs as well in humans.The authors emphasized the similarity between Shwartzman phenomenon and acute pancreatitis and suggest that heparin should be used in the prevention and treatment of acute pancreatitis in human.
Properties of Thrombin and Fibrinogen
Authors: Baughman D. J , Waugh D. F , Juvkam-Wold Constance 
Published: June 2018

SummaryA standard clotting system has been analysed according to the average clotting time and variations due to thrombin, fibrinogen, day-to-day preparation of reagents and the clotting assay itself. The variations, εT, εF and ετ are reproducible and normally distributed with zero mean.Transfer of thrombin into a vessel produces adsorption losses at the solution-air (S/A) and solution-wall (S/W) interfaces. Specific loss at τ = 30 sec = (% loss in τ) (thrombin volume)/surface area. For clean non-polar surfaces such as polyethylene or paraffin the average S/W loss of 3.8%-cm (0.77 mg/m2) has the large coefficient of variation of 3.2%. Vessel surfaces may be saturated by prior conditioning using a thrombin concentration tenfold that required to give τ = 50 sec. Emptying and immediately refilling now gives an S/W loss of 0.19%-cm (0.04 mg/m2). The specific S/A loss, always present, is 2.7%-cm (0.54 mg/m2). The combined average loss for conditioned vessels is 1.0% at τ = 30 sec and is reproducible within sτ
2 for single vessels. A set of vessels gives a coefficient of variation of 0.53%.Stock fibrinogen aliquots are stored frozen at —95° and are thawed and diluted under standard conditions. If a syringe is used to withdraw clotting tube aliquots, SF2 is significantly increased over that obtained by using pipettes. Since pipettes do not contribute, the observed coefficient of variation of 1.7% then applies to the variation between tubes of stock-F. Six different lots of Fraction I gave a coefficient of variation of 12% between lot numbers.Experiments revealed a variance between equivalent experiments performed on different days (coefficient of variation 1.9%). Within this variance pairs of stock reagents were stable within the maximum limits of ± 0.12% of τ per day. There is no reason to suspect that either stock reagent has an intrinsic instability. The day-to-day variance given above arises from non-reproducibilities in the preparation of buffer diluents. Variances were reduced when buffers were prepared in deaerated water at room temperature.The total day-to-day coefficient of variation of fibrinogen of 1.5% and the variation between fibrinogen lots effectively eliminates this reagent as a reference standard. Thrombin appeared otherwise : by selecting and reusing reservoirs the maximum total thrombin day-to-day coefficient of variance is 0.36%. Thus, 95% of the thrombin concentrations prepared on different days will lie within 0.72% of the true value. By making use of known purification procedures it is possible to reproduce a stock thrombin reagent. This would serve as a universal standard.
Thrombin - Fibrinogen Clotting Times
Authors: Waugh D. F , Baughman D Joe , Juvkam-Wold Constance 
Published: June 2018

SummaryThe fundamental variation to be taken into consideration in comparing clotting time averages is that of the clotting time assay itself. A variation is ετ whose true variance is στ
2 and the experimental estimate of this variance sτ
2. Described is a clotting time machine automated with respect to temperature, thrombin volume, thrombin injection, stirring and time determination so that the only subjective observation is that of the clotting time endpoint. Statistical analysis of sτ
2 has been made using protocols in which measurements either were carried out in a particular time sequence (regression type protocol) or were randomized (randomization type). An experimental unit is a dilute thrombin solution, a dilute fibrinogen solution and an operator-machine. The dilute reagents come from stock reagents. Characteristics of the system are as follows. 1. For a wide variety of experimental units the ετ are time independent and normally distributed. The sτ
2 from single lots of stock reagents appear to be estimates of the same στ
2. If different stock reagents are used the measured sτ
2 show that στ
2 may change significantly. 2. The variance increases with the clotting time. An approximate square relationship has been used for normalization. 3. The operator-machine and dilute solutions of stock thrombin appear to be remarkably uniform. 4. A change in στ
2 between experimental units is due to fibrinogen and appears particularly when different lots of fibrinogen, Armour’s Fraction I, are used to prepare the purified stock reagent. 5. When time dependent changes occur in experimental units, they are also most likely due to fibrinogen instability. When the storage temperature of stock-F is decreased from —20° to —95°, fibrinogen solubility is stabilized and regression decreased. 6. When instabilities can be made small, a randomization type protocol is preferred since fewer clotting times are required to characterize an experimental unit. When instability is important, a number of assays must be invested in its detection. This number increases approximately linearly with sτ
2 and decreases linearly as the time period for assays increases. The most important limitation to the examination of regressions is the number of clotting times an observer can perform on a single day.