The Role of Blood Platelets in the Precipitation of Soluble Fibrin by Endotoxin

Eckhardt, Thomas; Müller‐Berghaus, Gert

doi:10.1111/j.1600-0609.1975.tb00315.x

Cited by 14 publications

(3 citation statements)

References 22 publications

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“…In contrast, coarse fibrinous microthrombi which do not show any platelet inclusions, but are exclusively composed of period-coincidentally aggregated clumsy fibrillar bundles, without signs of a trellis pattern, are generated from a primary precipitation of soluble intermediates of the fibrinogen-fibrin conversion under the conditions of prestasis or stasis. Without doubt, this formation does not depend on the participation of platelet aggregates, but also occurs in thrombocytopenic test animals [26]. The morphogenesis of these coarse, primary fibrinous microthrombi parallels the morphogenesis of highly polymerized fibrinous clots in the test tube.…”

Section: Coarse Hyaline Microthrombimentioning

confidence: 84%

“…On one hand, soluble fibrinogen-fibrin monomer complexes are looked upon as the morphologic equivalent of a plasmatic hypercoagulability. On the other hand, high molecular weight fibrin degradation products are symptoms of a plasmin-induced fibrin olysis [26,49,54,71]. Like fibrinogen, high-molecular weight degradation products may aggregate with plasmatic fibrin monomers in vivo and in vitro and form soluble fibrin monomer-fibrin degradation product complexes.…”

Section: Fibrin Monomer and Fibrin Oligomermentioning

confidence: 99%

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Morphologic Diagnosis of Disseminated Intravascular Coagulation: Histologic, Histochemical and Electronmicroscopic Studies

Bleyl¹

2008

Semin Thromb Hemost

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The syndrome "disseminated intravascular coagulation" (DIC) is an "inter mediary mechanism of disease" [57] initiated by a local or generalized activation of coagulation and characterized by the dynamics of an enhanced consumption of procoagulant as well as anticoagulant coagulation factors ["consumption coagulo pathy," 42, 43]. The consumption involves not only the plasmatic but also the thrombocytic coagulation factors.The consumption of platelets and platelet factors already occurs during the initial phase of DIC and is characterized by the formation of platelet-rich microthrombi in the peripheral circulation and by the embolization of these microthrombi. In contrast, the consumption proper of the procoagulant and anticoagulant plasmatic coagulation factors, except the tissue plasminogen acti vator [5,21,31], cannot be histomorphologically visualized. Thus the decisive histomorphologic symptom of a preceding plasmatic consumption is provided by characteristic morphologic changes that only concern fibrinogen and its high molecular weight derivatives during the final phase of DIC. PLATELET-RICH MICROTHROMBIIn the initial stages of DIC, platelet-rich microthrombi are particularly observed in the capillaries of the lungs [4,33,44,52]. The lungs can be considered as a filter for all platelet aggregates which are generated in the microcirculation or in the venous blood (Fig. 1). The pulmonary clearance of platelets has been termed "trapping of the platelets by the lungs."Three pathophysiologic phases can normally be distinguished: In the course of the first phase, platelets aggregate reversibly or adhere to the surface of endothelial cells. In a second phase, these platelets can either disaggregate or form irreversible accumulations with consecutive viscous metamorphosis. It is only during this second phase that vasoactive substances and procoagulative material are released into the surrounding medium [4,35,61,63,67,81]. In the third phase, platelet-rich microthrombi can convert to fibrin-rich microthrombi after destruc tion of platelets and inhibition of platelet aggregates by plasma factors [41,69,70].

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Section: Coarse Hyaline Microthrombimentioning

confidence: 84%

Section: Fibrin Monomer and Fibrin Oligomermentioning

confidence: 99%

Morphologic Diagnosis of Disseminated Intravascular Coagulation: Histologic, Histochemical and Electronmicroscopic Studies

Bleyl¹

2008

Semin Thromb Hemost

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“…The release of these precipitating factors can be induced by endotoxin in vitro as well as in vivo. Experiments in the rabbit, however, have shown that platelets are not involved in the precipitation of soluble fibrin mediated by endotoxin, as thrombocytopenia did not prevent the occurrence of microclot formation [37,176]. Thrombocytopenia was induced either by platelet antiserum or by busulphan (Table 9).…”

Section: (A) Platelets and Precipitation And/or Polymerization Of Solmentioning

confidence: 99%