The kinin system: its relation to blood coagulation, fibrinolysis and the formed elements of the blood

Movat, Henry Z.

doi:10.1007/bfb0030492

Cited by 18 publications

(9 citation statements)

References 262 publications

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“…Cell membranes get reorganized in a sense that the cells might get leaky [39]. The contact system of human hemostasis is of enormous importance in many different diseases [48][49][50][51][52][53], kallikrein being a multitalented enzyme that not only activates factor 12 or factor 11 but also, for example, prourokinase, factor 10, or prothrombin [54][55][56]. So, 'surface energy' could directly fold factor 12 into factor 12a [41] or prekallikrein into kallikrein or it could change the cell ambience that then could activate these contact triggers [42][43][44][45][46][47].…”

Section: Resultsmentioning

confidence: 99%

Diagnostic ultrasound activates pure prekallikrein

Stief¹,

Klingmüller

2012

Blood Coagulation &Amp; Fibrinolysis

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Diagnostic ultrasound activates the contact phase of human coagulation. This has been seen in human blood or plasma or with purified factor 12. The present work aimed to quantify a possibly triggering action of ultrasound on purified prekallikrein, the second of the two main triggers of the intrinsic hemostasis cascade. Either 2.7 μg/ml human prekallikrein or for control 1 μg/ml kallikrein in 26% glycerol - 0.54% NaCl-10.6 mmol/l Na3 citrate pH 7.4, in emptied polypropylene coagulation monovettes (Sarstedt) were exposed to diagnostic ultrasound (Siemens Acouson Antares, 5 MHz, 0.6 TIB, 0.6 TIS) for 0-5 min at room temperature (RT). Fifty microliter samples were withdrawn in duplicate and placed into an U-wells high quality microtiter plate (Brand 781600). Then 10 μl 2 mmol/l chromogenic substrate HD-CHG-Ala-Arg-pNA in 0.45% NaCl were added, and the increase in absorbance with time (ΔA405 nm /t at 37°C) was determined by a microtiterplate photometer with a 1 mA resolution (PHOmo; anthos). Exposure to diagnostic ultrasound biphasically increased the chromogenic activity of a prekallikrein solution in 26% glycerol. About 3-4 min ultrasound at 23 °C generated about 0.02 μg/ml kallikrein, that means that about 1% of pure prekallikrein in glycerol was converted into kallikrein. Thus, diagnostic ultrasound activates purified human prekallikrein to kallikrein. The ultrasound energy seems to fold the latent proenzyme prekallikrein into the active enzyme kallikrein. This contributes to explain the triggering action of ultrasound on the contact system of plasmatic human coagulation. Conversion of only 1% of prekallikrein into kallikrein is absolutely sufficient to start the intrinsic coagulation cascade. The clinical consequence of this action of ultrasound on intrinsic coagulation is that patients at risk for thrombosis, for example, patients with insufficiencies of hepatocytes, AT-3, C1-ina, or fibrinolysis should be protected by low-molecular-weight-heparin prior to the exposure of ultrasound, especially upon its prolonged exposure.

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Section: Resultsmentioning

confidence: 99%

Diagnostic ultrasound activates pure prekallikrein

Stief¹,

Klingmüller

2012

Blood Coagulation &Amp; Fibrinolysis

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“…The deposition of fibrin is likely to contribute, in general, to the induration characteristic of inflammatory responses, such as delayed type hypersensitivity reactions (14); in addition, cells such as macrophages, which have receptors for fibrin (15), might be trapped at a site by a fibrin deposit. Kinins have been shown to have certain activities relevant to inflammation, for example, dilation of blood vessels, increase in vascular permeability and pain induction (1). In this context, Suzuki and Churg (12) have described the exudation of edema fluid in alveolar spaces soon after intratracheal injection of chrysotile fibers into hamsters (indicating an increase in vascular permeability), vascular modifications including venous dilation have been elicited in the hamster cheek pouch by asbestos fibers (16) and the hyperemia induced in rabbit skin by asbestos fibers has been quantitated (17 Sample Number to fibrin deposition and kinin liberation, the activation of factor XII can lead to the activation of the complement system, plasmin formation and the generation of bioactive fragments from fibrinogen and fibrin (1).…”

Section: Discussionmentioning

confidence: 99%

“…The animals were sacrificed and the horns of the uterus removed. One of the horns was opened lengthwise and suspended in a 5.0-mL tissue bath containing oxygenated de Jalon solution, pH 7.4, at 290C, with 1 The total concentration of kinin (ng/mL) present was calculated by multiplying the dilution factor by the equivalent response obtained (5). The range of variation from the duplicate samples was < 5%.…”

Section: Partial Thromboplastin Time (Ptt)mentioning

confidence: 99%

“…Many negatively charged surfaces can cause plasma to clot, with activation of factor XII being an early step in the activation of the so-called intrinsic coagulation cascade (1). Fibrin clots have been detected at sites of inflammation (2), while several putative mediators of inflammation, for example, kinins and the products of the fibrinolytic pathway, can also result from the activation of factor XII (1). Since asbestos fibers have charged surfaces, the interaction of these fibers with human plasma was examined.…”

Section: Introductionmentioning

confidence: 99%

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Asbestos Fibers, Plasma and Inflammation

Hamilton¹

1983

Environmental Health Perspectives

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Fibrin clots have been detected at sites of inflammation, and kinins have been implicated as mediators of the vascular phenomena of acute inflammation, systemic shock, and disseminated intravascular coagulation. It is now reported that both negatively and positively charged asbestos fibers shorten the partial thromboplastin time of human plasma, indicating coagulation of the plasma. A sample containing short (<5 Mm in length) chrysotile fibers is ineffective. Only the negatively charged amphiboles (crocidolite and amosite) are able to activate factor XII (Hageman factor). This particular effect of the amphiboles is enhanced by high molecular weight kininogen and leads to kinin formation.

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“…The thrombus formation in the renal vascular bed as a mecha nical obstruction of the lumen and the vasoactive sub stances released during platelet activation [20] might change the renal hemodynamics. Although the renal hyperfibrino(geno)lysis suppresses coagulation, it per se may exert a complex vascular response: plasmin is known to activate Hageman factor, plasma prekallikrein [21] and the complement system [22], thus to release bradykinin and anaphylatoxin. In addition to this, FDP potentiate the effects of bradykinin, angiotensin II, histamine, serotonin, acethylcholine and catecholamines [23], The pathogenetic role of coagulation and hyperfibrinolysis should be studied with their separate and simultaneous inhibition.…”

Section: Discussionmentioning

confidence: 99%

Simultaneous Activation of Coagulation and Fibrinolysis after Severe Renal Ischemia in Rats

Losonczy¹,

Harsing²

1982

Nephron

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Coagulation and fibrinolysis were studied during and after bilateral renal artery occlusion for 2 h in rats. After the release of the arterial clamps platelet count and plasma fibrinogen concentration decreased and circulating fibrin monomers were detected. The shortening of euglobulin lysis time and the accumulation of fibrinogen/fibrin degradation products indicated a simultaneous activation of fibrinolysis. Rapid and severe hemolysis was evident by the steadily increasing plasma hemoglobin concentration. Bilateral nephrectomy reversed all these pathological changes.

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The kinin system: its relation to blood coagulation, fibrinolysis and the formed elements of the blood

Cited by 18 publications

References 262 publications

Diagnostic ultrasound activates pure prekallikrein

Diagnostic ultrasound activates pure prekallikrein

Asbestos Fibers, Plasma and Inflammation

Simultaneous Activation of Coagulation and Fibrinolysis after Severe Renal Ischemia in Rats

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