scholarly journals ON THE NATURE OF FORCES OPERATING IN BLOOD CLOTTING

1945 ◽  
Vol 29 (2) ◽  
pp. 103-112 ◽  
Author(s):  
W. F. H. M. Mommaerts
Keyword(s):  
Ionic Radius ◽  
Blood Clotting ◽  
Electrostatic Attraction ◽  
Inhibiting Effect

The results of the study of the inhibiting effect of neutral salts upon the clotting tendency of fibrinogen by thrombin may be summarised as follows: Salts like NaCl and KCl inhibit only weakly. Salts of the same cation (K•) with monovalent anions of different ionic radius are the more active the larger the anion (Cl',Br',I'). Salts of the same cation with anions of different valency are the more active the higher the charge of the anion (1–1 <1–2 <1–3 <1–4). Salts with the same anion with cations of different valency show stronger inhibition in the case of cations of higher charge (K•,Na• < Mg••, Ca••, Sr••, Ba••). Salts with the same anion and cations of the same charge, but of different radius, are the more active the larger the cation (but with an inversion between Mg•• and Ca•• in the series of the alkali earths, which is not infrequent in biocolloids). These results show that the clotting of fibrinogen with thrombin is, at least partly, caused by a coacervation process, due to electrostatic attraction between positive and negative groups. Its nature and localisation will be dealt with in the next paper of this series.

scholarly journals ON THE NATURE OF FORCES OPERATING IN BLOOD CLOTTING

1945 ◽  
Vol 29 (2) ◽  
pp. 113-122 ◽  
Author(s):  
W. F. H. M. Mommaerts
Keyword(s):  
Hydrogen Bonds ◽  
Isoelectric Point ◽  
Blood Clotting ◽  
Electrostatic Attraction ◽  
Primary Reaction ◽  
Ph Values ◽  
Positively Charged

It is found that clotting of fibrinogen by thrombin does not occur on the acid side of the isoelectric point of the fibrinogen. At such pH values, however, a primary reaction between thrombin and fibrinogen takes place, leading to the formation of profibrin, a compound of thrombin and fibrinogen. At pH values at which clotting is possible, fibrinogen is negatively, thrombin positively charged, whereas profibrin has a pattern of positive and negative charges. The primary reaction, the formation of profibrin by combination of thrombin and fibrinogen, is inhibited by urea but not by neutral salts. The combination of thrombin with fibrinogen most probably takes place by hydrogen bonds. The second reaction, the polymerisation of profibrin to fibrin, is inhibited by neutral salts in the same way as complex or autocomplex coacervates. It is caused therefore by electrostatic attraction between the positive and the negative charges of the profibrin.

Effects of dopant concentration on the microstructure of tin- doped indium oxide thin films

1990 ◽  
Vol 48 (4) ◽  
pp. 716-717
Author(s):  
I. A. Rauf
Keyword(s):  
Thin Films ◽  
Indium Oxide ◽  
Ionic Radius ◽  
Free Carrier ◽  
Electron Gun ◽  
Periodic Lattice ◽  
Oxide Thin Films ◽  
Transmission Electron ◽  
The Difference ◽  
Dopant Atoms

To understand the electronic conduction mechanism in Sn-doped indium oxide thin films, it is important to study the effect of dopant atoms on the neighbouring indium oxide lattice. Ideally Sn is a substitutional dopant at random indium sites. The difference in valence (Sn4+ replaces In3+) requires that an extra electron is donated to the lattice and thus contributes to the free carrier density. But since Sn is an adjacent member of the same row in the periodic table, the difference in the ionic radius (In3+: 0.218 nm; Sn4+: 0.205 nm) will introduce a strain in the indium oxide lattice. Free carrier electron waves will no longer see a perfect periodic lattice and will be scattered, resulting in the reduction of free carrier mobility, which will lower the electrical conductivity (an undesirable effect in most applications).One of the main objectives of the present investigation is to understand the effects of the strain (produced by difference in the ionic radius) on the microstructure of the indium oxide lattice when the doping level is increased to give high carrier densities. Sn-doped indium oxide thin films were prepared with four different concentrations: 9, 10, 11 and 12 mol. % of SnO2 in the starting material. All the samples were prepared at an oxygen partial pressure of 0.067 Pa and a substrate temperature of 250°C using an Edwards 306 coating unit with an electron gun attachment for heating the crucible. These deposition conditions have been found to give optimum electrical properties in Sn-doped indium oxide films. A JEOL 2000EX transmission electron microscope was used to investigate the specimen microstructure.

Evidence for an Increased Generation of Prostacyclin in the Microvasculature and an Impairment of the Platelet α-Granule Release in Chronic Renal Failure

1988 ◽  
Vol 60 (02) ◽  
pp. 205-208 ◽  
Author(s):  
Paul A Kyrle ◽  
Felix Stockenhuber ◽  
Brigitte Brenner ◽  
Heinz Gössinger ◽  
Christian Korninger ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Blood Clotting ◽  
Normal Subjects ◽  
Chronic Uraemia ◽  
Wall Interaction ◽  
End Stage ◽  
Granule Release

SummaryThe formation of prostacyclin (PGI2) and thromboxane A2 and the release of beta-thromboglobulin (beta-TG) at the site of platelet-vessel wall interaction, i.e. in blood emerging from a standardized injury of the micro vasculature made to determine bleeding time, was studied in patients with end-stage chronic renal failure undergoing regular haemodialysis and in normal subjects. In the uraemic patients, levels of 6-keto-prostaglandin F1α (6-keto-PGF1α) were 1.3-fold to 6.3-fold higher than the corresponding values in the control subjects indicating an increased PGI2 formation in chronic uraemia. Formation of thromboxane B2 (TxB2) at the site of plug formation in vivo and during whole blood clotting in vitro was similar in the uraemic subjects and in the normals excluding a major defect in platelet prostaglandin metabolism in chronic renal failure. Significantly smaller amounts of beta-TG were found in blood obtained from the site of vascular injury as well as after in vitro blood clotting in patients with chronic renal failure indicating an impairment of the a-granule release in chronic uraemia. We therefore conclude that the haemorrhagic diathesis commonly seen in patients with chronic renal failure is - at least partially - due to an acquired defect of the platelet a-granule release and an increased generation of PGI2 in the micro vasculature.

The Basis of the Cascade Hypothesis of Blood Clotting

1966 ◽  
Vol 15 (03/04) ◽  
pp. 591-602 ◽  
Author(s):  
R. G Macfarlane
Keyword(s):  
Blood Clotting

Kinetic Aspects of the Interaction of Blood-Clotting Enzymes

1968 ◽  
Vol 20 (01/02) ◽  
pp. 078-087 ◽  
Author(s):  
H. C Hemker ◽  
A. D Muller
Keyword(s):  
Vitamin K ◽  
Blood Clotting ◽  
Experimental Results ◽  
Factor X ◽  
Clotting Factors ◽  
Vitamin K Deficiency ◽  
K Deficiency

SummaryPIVKA, the circulating anticoagulant protein found in vitamin K deficiency can, on kinetical grounds, be recognized as an analogue of factor X. The existence of analogues of other vitamin K-dependent clotting factors cannot be ruled out, but need not be assumed to explain the experimental results.

Kinetic Aspects of the Interaction of Blood Clotting Enzymes

1968 ◽  
Vol 19 (03/04) ◽  
pp. 364-367 ◽  
Author(s):  
H. C Hemker ◽  
P. W Hemker
Keyword(s):  
Enzyme Kinetics ◽  
Blood Clotting ◽  
Competitive Inhibition ◽  
Competitive Inhibitor ◽  
Kinetics Of

SummaryThe enzyme kinetics of competitive inhibition under conditions prevailing in clotting tests are developed and a method is given to measure relative amounts of a competitive inhibitor by means of the t — D plot.

Hypercoagulability Syndrome Due to Heparin Co-Factor Deficiency

1964 ◽  
Vol 11 (02) ◽  
pp. 485-496 ◽  
Author(s):  
B. J Koszewski ◽  
H Vahabzadeh
Keyword(s):  
Dynamic Process ◽  
Blood Clotting ◽  
Complete Recovery ◽  
Inhibition Test ◽  
Factor Deficiency ◽  
Heparin Resistance ◽  
Fever Therapy ◽  
Intensive Course ◽  
Plasma Infusions

SummaryA case of hypercoagulability syndrome in a 35 years old male is reported. An abnormal heparin resistance was found which could be defined by means of a heparin clot-inhibition test as a deficiency in heparin co-factor. The required anticoagulant doses of heparin were forty times as high as in cases with intact heparin co-factor. The factor seemed to be used up in the process of coagulation, as plasma, but not serum, was able to correct the deficiency in vitro. Plasma infusions were helpful for four days, but a complete recovery was achieved only after an intensive course of fever therapy.The phenomenon of blood clotting should be regarded as a dynamic process which is facilitated by an array of clot promoting factors and opposed by a system of natural anticoagulants.

Blood Coagulation Studies and Extracorporeal Circulation in Man

1967 ◽  
Vol 18 (03/04) ◽  
pp. 634-646 ◽  
Author(s):  
N Thurnherr
Keyword(s):  
Blood Coagulation ◽  
Extracorporeal Circulation ◽  
Blood Clotting ◽  
Heart Surgery ◽  
Open Heart Surgery ◽  
Fibrinolytic System ◽  
Open Heart ◽  
Clotting Factors ◽  
Blood Clotting Factors

SummaryBlood clotting investigations have been executed in 25 patients who have undergone open heart surgery with extracorporeal circulation. A description of alterations in the activity of blood clotting factors, the fibrinolytic system, prothrombin consumption and platelets during several phases of the operation is given.

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