Globular hyaline microthrombi ? Their nature and morphogenesis

Bleyl, U.; Roßner, J. A.

doi:10.1007/bf00430808

Cited by 20 publications

(15 citation statements)

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“…Globuli of this type have been described by other authors and are believed to be composed mainly of fibrin and fibrin degra dation products [5,30], They have been ob served in human shock cases, especially in endotoxin shock, and most often in the lungs.…”

Section: Discussionmentioning

confidence: 98%

Aggregate Anaphylaxis in the Monkey

Smedegård¹,

Revenäs²,

Saldeen³

1980

Int Arch Allergy Immunol

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Haematological and histological studies were made following challenge in 8 monkeys (Macaca irus) sensitized with ovalbumin. Haemagglutinating, but no reaginic antibodies to ovalbumin were demonstrated before challenge. Both platelet and leucocyte counts decreased markedly (––80 and ––89%, respectively) within 5 min after challenge. No evidence of haemoconcentration was found. Plasma fibrinogen decreased (––74%), indicating activation of the coagulation system. Histological examination revealed platelets, leucocytes, fibrin and a large number of hyaline globuli (‘globular microemboli’) in pulmonary capillaries and small arterioles. From their staining properties the globuli were considered to consist mainly of fibrin. Some globuli were also found in the liver and kidneys, but were rarely seen in other organs. It is concluded that the anaphylactic reaction in this experimental model can be classified as aggregate anaphylaxis, and it is suggested that platelet mediators play an important role in the early pulmonary vascular and respiratory response.

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Section: Discussionmentioning

confidence: 98%

Aggregate Anaphylaxis in the Monkey

Smedegård¹,

Revenäs²,

Saldeen³

1980

Int Arch Allergy Immunol

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“…These globular hyaline microthrombi consist of variable dense, internetted fibrillar bundles, forming irregular spheric space lattices (Fig. 5), and surrounding variable large, electron microscopically empty spaces [14]. The fibrillar bundles show an extremely regular fibrin-characteristic axial striation [47] with a mean periodicity of 23 nm (19-25 nm) in those areas where the cut surface of the ultra-thin slices runs parallel to the filaments (Fig.…”

Section: Globular Hyaline Microthrombimentioning

confidence: 99%

“…Globular hyaline microthrombi [76] were described 80 years ago as fibrin balls [53], fibrin globules [1,2] or Siegmund-Schindler globules [75]. They must be considered morphologic equivalents of local or generalized activation of the plasmatic coagulation system, characterized by the in vivo generation of highly aggregated insoluble fibrin intermediates [14]. Globular hyaline microthrombi have a diameter of 3 -60 µ, sometimes even up to 100 µ.…”

Section: Globular Hyaline Microthrombimentioning

confidence: 99%

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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“…4.22). 18,[112][113][114][115][116] It is uncertain whether intravascular coagulation initiates lung injury, 73,117,118 but histamine released from platelets is likely to increase vascular permeability whilst fibrin degradation products, which are elevated in patients with the respiratory distress syndrome, 119 are known to induce pulmonary oedema. 120 Larger pulmonary thrombi, formed in situ or embolic, are common in patients with ARDS.…”

Section: Sepsis -The Systemic Inflammatory Response To Infectionmentioning

confidence: 99%