Aim. To study the effect of the blood components on clot contraction dynamics in vitro.Methods. The original method based on the optical detection of changes in the blood clot volume over time was used. Whole blood, as well as reconstructed samples using washed platelets, erythrocytes, purified fibrinogen, platelet-poor and platelet-rich plasma were studied.Results. Blood clot contraction has a non-linear kinetics, reflecting the complexity of the underlying mechanisms. Platelets increase the blood clot contraction, while the red blood cells have an inhibitory effect. Blocking the fibrin and platelets interaction using the RGDS peptide, an integrin αIIbβ3 antagonist, reduces the extent and rate of clot contraction. The exogenous Ca2+ is not required for contraction, but its addition stabilizes clots by inhibiting the erythrocytes. Thrombin has a dose-dependent effect and increases the rate and extent of contraction. In blood samples of patients taking warfarin, blood clot contraction was delayed.Conclusion. The blood clot contraction is a process which depends on many factors, including the blood cell composition, amount of fibrinogen, the endogenous thrombin activity and platelets interaction with fibrin; understanding the mechanisms of the blood clot contraction could form the basis for the development of novel approaches to the hemostatic disorders treatment.

РефератЦель. Установить, происходит ли in vivo контракция (ретракция) тромбов и тромботических эмболов, исполь-зуя структурные признаки сжатия сгустков крови: компрессионную деформацию эритроцитов и перераспреде-ление фибрина на поверхности сгустка. Методы. Исследовали 3 посмертных лёгочных тромботических эмбола методами сканирующей электронной микроскопии и световой микроскопии после окраски срезов гематоксилином-эозином и по методу Маллори. Результаты. В составе 2 исследованных лёгочных эмболов, извлечённых через 7 и 15 ч после смерти пациен-тов, обнаружены эритроциты в форме многогранника, или полиэдра («полиэдроциты»), которые образуются в результате механической деформации под действием контрактильных сил, генерируемых активированны-ми тромбоцитами. Кроме того, выявлено неравномерное распределение фибрина внутри эмбола, проявляюще-еся вытеснением фибрина к периферии, что характерно для контрактированного сгустка крови. В 1, наиболее «старом» эмболе, извлечённом через 38 ч после смерти пациента, указанные признаки контракции отсутство-вали, что связано либо с посмертным аутолизом, либо с патологическим нарушением контракции при жизни. Вывод. Тромботические эмболы ex vivo имеют морфологические признаки контракции, свидетельствующие о прижизненном сжатии первичных тромбов и/или тромботических эмболов, что может быть важным патоге-нетическим механизмом восстановления нарушенного кровотока в очаге тромботической окклюзии сосуда; на-личие или отсутствие компрессированных эритроцитов внутри и преимущественное расположение фибрина по периферии тромба или эмбола потенциально могут служить дополнительными патоморфологическими крите-риями давности наступления смерти. Ключевые слова: тромбоз, тромбоэмболия, свёртывание крови, контракция сгустка, ретракция сгустка. Morphological signs of the intravital contraction (retraction) of thrombotic emboli University of Pennsylvania, Department of Cell and Developmental Biology of the School of Medicine, Philadelphia, USAAim. To establish whether contraction (retraction) of thrombi and thrombotic emboli occurs in vivo using structural signs of blood clot compression, such as compressive deformation of erythrocytes and redistribution of fibrin on the surface of a clot. Methods. Three postmortem pulmonary thrombotic emboli were examined by scanning electron microscopy and light microscopy after staining with hematoxylin and eosin as well as with Mallory's method. Results. In 2 studied pulmonary emboli, extracted 7 and 15 hours after patients' death, polyhedral erythrocytes (polyhedrocytes) were revealed that were formed as a result of mechanical deformation under the action of contractile forces generated by activated platelets. In addition, the uneven distribution of fibrin within the emboli was found with displacement of fibrin to the periphery of the emboli, which is characteristic for contracted blood clot. In the first and the «oldest» clot extracted 38 hours after the patient's death, the described contraction signs were absent, which was likely related to the postmortem au...

Aim. To describe a case of arterial thrombosis with a thrombus that had atypical composition due to profound pathological changes in the cellular and protein composition of the blood. Methods. Scanning electron microscopy of an ex vivo thrombus extracted from the common femoral artery. Results. In the absence of platelets and leukocytes there was a significant prevalence of fibrin over other blood components in all layers of the arterial thrombus. There were no morphological signs of intravital contraction (retraction) characteristic for thrombi: single erythrocytes were not exposed compressive deformation, redistribution of fibrin and platelets within the thrombus toward the periphery. Formation of the atypical arterial thrombus in the vessel with atherosclerotic vessel damage is probably due to association with severe hyperfibrinogenemia and thrombocytopenia. Conclusion. The structure of a thrombus depends not only on its vascular location (arterial or venous), but also on the cellular and protein composition of the blood. These factors support diversification of antithrombotic therapy, considering composition and properties of thrombi irrespective of the place and hemodynamic conditions of their formation.