Background: The development of disseminated intravascular coagulation syndrome (DIC), with liver pathologies, is usually considered a terminal condition caused by a violation of the blood coagulation system. A number of blood coagulation factors are synthesized by the liver, in this regard, the development of DIC syndrome in liver pathology is of particular importance. It is assumed that the DIC syndrome in liver pathology is caused by a violation of the coagulation properties of the blood. At the same time, local lesions of the hematocirculatory bed of the liver, as well as ultrastructural aspects of intravascular blood coagulation, remain unclear. Objective: To study the hematocirculatory bed of the liver and the features of the ultrastructure of platelet thrombi at 20-day experimental cholestasis in experimental white rats. Materials and methods: Experimental cholestasis was created in experimental rats (m=28) by ligation and transection of the common bile duct. The animals were sacrificed in compliance with ethical standards on days 10 and 20 of cholestasis. The liver tissue was examined by histological, corrosive, and electron microscopic methods. Results: Studies have shown that the development of DIC occurs with 20-day cholestasis, when biliary cirrhosis is formed in the liver. Some disorders of hemocirculation are observed at 10 days of cholestasis, in the form of erythrocyte sludge in the vessels of the liver. A pronounced disseminated intravascular coagulation syndrome manifests itself at 20 days of cholestasis. Disturbance of circulation is expressed in the interlobular branches of the portal system. Formed thrombi consist mainly of platelets with a minor admixture of erythrocytes and leukocytes. Ultrastructurally, a thrombus appears to be aggregated platelets, the structure of which is without significant changes. The elements of the hyalomer and granulomere are well detected in them. Most contain dense granules, some have undergone degranulation. A distinctive feature of a thrombus is the absence of fibrin filaments in the thrombus. Conclusion: Long-term experimental cholestasis, in some cases, is accompanied by a violation of the anticoagulant properties of the blood and contributes to the development of DIC. The morphological manifestation of which are platelet thrombi that arise in the interlobular veins. The ultrastructural features of these thrombi indicate an increase in the aggregation capacity of platelets, which, in combination with impaired hemostasis, probably contributes to the development of hemorrhage in liver pathology.
| Published in | International Journal of Clinical and Experimental Medical Sciences (Volume 7, Issue 5) |
| DOI | 10.11648/j.ijcems.20210705.12 |
| Page(s) | 138-142 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
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Copyright © The Author(s), 2024. Published by Science Publishing Group |
Liver, Obstructive Jaundice, Intravascular Blood Coagulation, Platelet Thrombus Ultrastructure
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APA Style
Sadriddinov Asomidin Faizovich, Sheraliev Kambarali Saidalievich. (2021). Morphological Bases of DIC Syndrome in the Liver with Biliary Obstruction. International Journal of Clinical and Experimental Medical Sciences, 7(5), 138-142. https://doi.org/10.11648/j.ijcems.20210705.12
ACS Style
Sadriddinov Asomidin Faizovich; Sheraliev Kambarali Saidalievich. Morphological Bases of DIC Syndrome in the Liver with Biliary Obstruction. Int. J. Clin. Exp. Med. Sci. 2021, 7(5), 138-142. doi: 10.11648/j.ijcems.20210705.12
AMA Style
Sadriddinov Asomidin Faizovich, Sheraliev Kambarali Saidalievich. Morphological Bases of DIC Syndrome in the Liver with Biliary Obstruction. Int J Clin Exp Med Sci. 2021;7(5):138-142. doi: 10.11648/j.ijcems.20210705.12
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Download@article{10.11648/j.ijcems.20210705.12,
author = {Sadriddinov Asomidin Faizovich and Sheraliev Kambarali Saidalievich},
title = {Morphological Bases of DIC Syndrome in the Liver with Biliary Obstruction},
journal = {International Journal of Clinical and Experimental Medical Sciences},
volume = {7},
number = {5},
pages = {138-142},
doi = {10.11648/j.ijcems.20210705.12},
url = {https://doi.org/10.11648/j.ijcems.20210705.12},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijcems.20210705.12},
abstract = {Background: The development of disseminated intravascular coagulation syndrome (DIC), with liver pathologies, is usually considered a terminal condition caused by a violation of the blood coagulation system. A number of blood coagulation factors are synthesized by the liver, in this regard, the development of DIC syndrome in liver pathology is of particular importance. It is assumed that the DIC syndrome in liver pathology is caused by a violation of the coagulation properties of the blood. At the same time, local lesions of the hematocirculatory bed of the liver, as well as ultrastructural aspects of intravascular blood coagulation, remain unclear. Objective: To study the hematocirculatory bed of the liver and the features of the ultrastructure of platelet thrombi at 20-day experimental cholestasis in experimental white rats. Materials and methods: Experimental cholestasis was created in experimental rats (m=28) by ligation and transection of the common bile duct. The animals were sacrificed in compliance with ethical standards on days 10 and 20 of cholestasis. The liver tissue was examined by histological, corrosive, and electron microscopic methods. Results: Studies have shown that the development of DIC occurs with 20-day cholestasis, when biliary cirrhosis is formed in the liver. Some disorders of hemocirculation are observed at 10 days of cholestasis, in the form of erythrocyte sludge in the vessels of the liver. A pronounced disseminated intravascular coagulation syndrome manifests itself at 20 days of cholestasis. Disturbance of circulation is expressed in the interlobular branches of the portal system. Formed thrombi consist mainly of platelets with a minor admixture of erythrocytes and leukocytes. Ultrastructurally, a thrombus appears to be aggregated platelets, the structure of which is without significant changes. The elements of the hyalomer and granulomere are well detected in them. Most contain dense granules, some have undergone degranulation. A distinctive feature of a thrombus is the absence of fibrin filaments in the thrombus. Conclusion: Long-term experimental cholestasis, in some cases, is accompanied by a violation of the anticoagulant properties of the blood and contributes to the development of DIC. The morphological manifestation of which are platelet thrombi that arise in the interlobular veins. The ultrastructural features of these thrombi indicate an increase in the aggregation capacity of platelets, which, in combination with impaired hemostasis, probably contributes to the development of hemorrhage in liver pathology.},
year = {2021}
}
TY - JOUR T1 - Morphological Bases of DIC Syndrome in the Liver with Biliary Obstruction AU - Sadriddinov Asomidin Faizovich AU - Sheraliev Kambarali Saidalievich Y1 - 2021/10/12 PY - 2021 N1 - https://doi.org/10.11648/j.ijcems.20210705.12 DO - 10.11648/j.ijcems.20210705.12 T2 - International Journal of Clinical and Experimental Medical Sciences JF - International Journal of Clinical and Experimental Medical Sciences JO - International Journal of Clinical and Experimental Medical Sciences SP - 138 EP - 142 PB - Science Publishing Group SN - 2469-8032 UR - https://doi.org/10.11648/j.ijcems.20210705.12 AB - Background: The development of disseminated intravascular coagulation syndrome (DIC), with liver pathologies, is usually considered a terminal condition caused by a violation of the blood coagulation system. A number of blood coagulation factors are synthesized by the liver, in this regard, the development of DIC syndrome in liver pathology is of particular importance. It is assumed that the DIC syndrome in liver pathology is caused by a violation of the coagulation properties of the blood. At the same time, local lesions of the hematocirculatory bed of the liver, as well as ultrastructural aspects of intravascular blood coagulation, remain unclear. Objective: To study the hematocirculatory bed of the liver and the features of the ultrastructure of platelet thrombi at 20-day experimental cholestasis in experimental white rats. Materials and methods: Experimental cholestasis was created in experimental rats (m=28) by ligation and transection of the common bile duct. The animals were sacrificed in compliance with ethical standards on days 10 and 20 of cholestasis. The liver tissue was examined by histological, corrosive, and electron microscopic methods. Results: Studies have shown that the development of DIC occurs with 20-day cholestasis, when biliary cirrhosis is formed in the liver. Some disorders of hemocirculation are observed at 10 days of cholestasis, in the form of erythrocyte sludge in the vessels of the liver. A pronounced disseminated intravascular coagulation syndrome manifests itself at 20 days of cholestasis. Disturbance of circulation is expressed in the interlobular branches of the portal system. Formed thrombi consist mainly of platelets with a minor admixture of erythrocytes and leukocytes. Ultrastructurally, a thrombus appears to be aggregated platelets, the structure of which is without significant changes. The elements of the hyalomer and granulomere are well detected in them. Most contain dense granules, some have undergone degranulation. A distinctive feature of a thrombus is the absence of fibrin filaments in the thrombus. Conclusion: Long-term experimental cholestasis, in some cases, is accompanied by a violation of the anticoagulant properties of the blood and contributes to the development of DIC. The morphological manifestation of which are platelet thrombi that arise in the interlobular veins. The ultrastructural features of these thrombi indicate an increase in the aggregation capacity of platelets, which, in combination with impaired hemostasis, probably contributes to the development of hemorrhage in liver pathology. VL - 7 IS - 5 ER -
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