Prostaglandin E1-induced deconsolidation of thrombin-activated platelet aggregates I : Ultrastructure-computer image analysis

We have compared, at an ultrastructural-computer image morphometric level, the relaxation induced by Mg-ethylene-bis-oxyethylenenitrilo-tetracetic acid and prostaglandin E1 on a model of a thrombin-activated platelet aggregate. Mg-ethylene-bisoxyethylenenitrilo-tetracetic acid produced a small incre...

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Veröffentlicht in:Thrombosis research 1999-06, Vol.94 (6), p.359-371
Hauptverfasser: SALGANICOFF, L, RUSSO, M. A, SEVY, R. W
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Sprache:eng
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Zusammenfassung:We have compared, at an ultrastructural-computer image morphometric level, the relaxation induced by Mg-ethylene-bis-oxyethylenenitrilo-tetracetic acid and prostaglandin E1 on a model of a thrombin-activated platelet aggregate. Mg-ethylene-bisoxyethylenenitrilo-tetracetic acid produced a small increase of 5.0% of the intercellular space over the control levels, and a decrease of 10.0+/-1.3% of the cross-sectional area of the platelets, with no apparent cytoskeletal alterations. In contrast, the prostaglandin El-treated preparation shows a 360% increase in the intercellular space and a decrease of the average platelet cross-sectional area of 30.0+/-2.0% with marked cytoskeletal alterations. We use the term "deconsolidation" to describe this effect. The enlargement of the intercellular space allows the observation of two types of contacts: (1) a type S (segmental) complex, of approximately 200-nm length that maintains a narrow interplatelet gap of 20-30 nm, filled with a dense intercellular material, and (2) a type R (reticular) complex, formed by scant focal regions of the plasma membrane from opposing platelets that are connected through a mesh of fibrillar or granular material contained within a variable-size space. We hypothesize that deconsolidation is caused by fluid loss from the platelets into the intercellular space. As a result, platelet volume decreases and intercellular space increases.
ISSN:0049-3848
1879-2472
DOI:10.1016/S0049-3848(99)00018-3