The Coagulation of blood

Mellanby, John

doi:10.1113/jphysiol.1909.sp001316

Cited by 79 publications

(21 citation statements)

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“…The thrombin preparations used were-except for one of bovine origin (Parke-Davisthrombin topical)-made from vario-us sources following essentially the proeedure introduced by Mellanby (1909): To one volume of oxalated plasma, diluted with nine volumes of. cold distilled water were added dropwise two volumes of 0-01 M citric acid, and well mixed.…”

Section: Methodsmentioning

confidence: 99%

The Interaction of Thrombin With the Plasma Components of Man and Experimental Animals

Fantl

Ebbels

1953

Aust J Exp Biol Med

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The addition of thrombin to blood plasma gives rise to several effects. One of them is the formation of fibringel. It is generally assumed that thrombin is the enzyme acting on the substrate fibrinogen. This is supported by experiments of Perry and Morrison (1947) who found that one part of a thrombin preparation could produce 10' parts of fibrin. If this calculation is applied to events in circulating blood it should mean that intravascular liberation of small quantities of thrombin should lead to complete clotting of all the blood in the body. However, such a result can be produced only by drastic experimental procedures. It is therefore obvious that most of the thrombin is consumed in reactions with components other than fibrinogen.This thrombin-disposing mechanism of plasma appears to be of complex nature. Fibrin can adsorb thrombin as has been recognized by Rettger (1909) and Howell (1910); and Seegers, Meft and Loomis (1945) have established the quantitative relationship of this adsorption. Finally, Schmidt (1892) observed that thrombin in defibrinated plasma or serum is unstable. Factors termed " antithrombin" are present. The quantitative aspect of this phenomenon has been investigated by several workers including Astrup and Darling (1943), Astrup (1947) and Klein and Seegers (1950). The ability of fibrin to adsorb thrombin and the activity of "antithrombin" are responsible for the disappearance of thrombin in blood.When thrombin is added to plasma of patients suffering from a variety of illnesses, including obstructive jaundice and multiple myelomata, it is often found that the clotting time is delayed when compared to plasma of normal persons, and a similar phenomenon is observed in the case of certain animal plasmas. The reason for this delay is not known. Since these phenomena have a bearing on problems related to haemorrhage, haemostasis and intravascular coagulation, relevant experiments were carried out and are reported.

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Section: Methodsmentioning

confidence: 99%

The Interaction of Thrombin With the Plasma Components of Man and Experimental Animals

Fantl

Ebbels

1953

Aust J Exp Biol Med

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“…This was confirmed by Mellanby (14) who injected, without thrombosis, sufficient thrombin into a cat to coagulate 2 litres of blood. After the intravascular injection of thrombin, Davis (15) found the coagulation time of shed blood to be variable, sometimes slightly lengthened at other times shortened.…”

Section: On the Supposed Formation And Secretion Of Antithrombin By Tmentioning

confidence: 83%

“…Two views have been advanced in this connection, viz., that of Martin (19), and of Barratt (20), where the active fraction of snake venom is considered to be a true fibrin-ferment (thrombin), and that of Melianby (21), that it is a kinase which, when rapidly injected, causes the rapid formation of thrombin. It is evident from the experiments of Artlius, that the " negative phase " of coagulation following either the rapid injection of minimal doses of venom, or the slow injection of larger doses, is not produced by the secretion by the liver of antithrombin, which combines with thrombin, either existing in, or produced by, venom.…”

Section: On the Supposed Formation And Secretion Of Antithrombin By Tmentioning

confidence: 99%

The action of "peptone" on blood and immunity thereto

1922

Proc. R. Soc. Lond. B.

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The current view on the cause of the non-coagulability of the blood after the injection of “peptone” is that the injected material stimulates the liver (or the liver plus other organs) to form an excess of a substance named antithrombin. The liver is considered further to form antithrombin under normal conditions in amount sufficient to maintain the fluidity of the blood. The statement that “peptone” which follows its slow injection is commonly ascribed to hepatic activity. The experiments recorded in this paper show that these views can no longer be held.

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“…This is natural, since the only test available for prothrombin is the conversion of the inactive precursor to thrombin. The methods previously employed for the preparation of crude thrombin (12, 104,148,150,189,190) will probably in the near future be completely superseded by procedures in which the highly purified prothrombin preparations, discussed in the preceding section, will be utilized. The ideal thrombin preparation, unrealized so far, would require a system consisting of physically and chemically homogeneous prothrombin of maximum potency and constant solubility, of calcium and of the pure thromboplastic protein (isolated from the same animal species as the particular prothrombin sample).…”

Section: Thrombinmentioning

confidence: 99%