Background:Knowing the variability of blood coagulation responses to liver damage of different origins can provide a key to curing liver tissues or to mitigating treatment side effects.The aim of the present work was ...Background:Knowing the variability of blood coagulation responses to liver damage of different origins can provide a key to curing liver tissues or to mitigating treatment side effects.The aim of the present work was to compare the changes in the main components of hemostasis under experimental drug-induced hepatosis and hepatitis in rats.Methods:We modeled diclofenac-induced hepatitis and tetracycline-induced hepa-tosis.Hemostasis response was gauged by measuring fibrinogen,factor X,protein C(PC),and prothrombin in plasma.The decarboxylated form of prothrombin was de-tected by measuring prothrombin index and ecamulin index.Platelet reactivity was studied using aggregometry.Results:Both hepatitis and hepatosis decreased the synthesis of fibrinogen,factor X,and prothrombin.However,protein carboxylation was not disrupted in hepatosis but was much impaired in hepatitis.PC decreased in both models as a consequence of its consumption possibly during inflammatory response.Platelet aggregation rate was lower in hepatosis but higher in hepatitis.Conclusions:Our findings imply the need for a thorough monitoring of the hemostasis system in liver diseases to avoid possible thrombotic complications.Its state indicates the disorder's rate and character.展开更多
Meizothrombin (MT) is one of prothrombin derivatives which appears in haemostasis activation area. However, its role in haemostasis regulation isn’t clear. We studied the role of MT in fibrin formation, platelet acti...Meizothrombin (MT) is one of prothrombin derivatives which appears in haemostasis activation area. However, its role in haemostasis regulation isn’t clear. We studied the role of MT in fibrin formation, platelet activation and aggregation. A new effective method of obtaining MT from native human prothrombin was developed using immobilised prothrombin activator from Echis multisquamatis venom. The protein was stable and electrophoretically pure. Platelet-rich plasma for aggregation study and gel-sieved platelets for flow-cytometry were separated from blood of healthy donors. It was shown that MT transformed fibrinogen to fibrin and activated clotting factor XIII. MT didn’t activate gel-sieved intact platelets, but in platelet-rich plasma, increased platelet aggregation induced by ADP, collagen and adrenalin.展开更多
基金National Academy of Sciences of Ukraine research,Grant/Award Number:0119U002512。
文摘Background:Knowing the variability of blood coagulation responses to liver damage of different origins can provide a key to curing liver tissues or to mitigating treatment side effects.The aim of the present work was to compare the changes in the main components of hemostasis under experimental drug-induced hepatosis and hepatitis in rats.Methods:We modeled diclofenac-induced hepatitis and tetracycline-induced hepa-tosis.Hemostasis response was gauged by measuring fibrinogen,factor X,protein C(PC),and prothrombin in plasma.The decarboxylated form of prothrombin was de-tected by measuring prothrombin index and ecamulin index.Platelet reactivity was studied using aggregometry.Results:Both hepatitis and hepatosis decreased the synthesis of fibrinogen,factor X,and prothrombin.However,protein carboxylation was not disrupted in hepatosis but was much impaired in hepatitis.PC decreased in both models as a consequence of its consumption possibly during inflammatory response.Platelet aggregation rate was lower in hepatosis but higher in hepatitis.Conclusions:Our findings imply the need for a thorough monitoring of the hemostasis system in liver diseases to avoid possible thrombotic complications.Its state indicates the disorder's rate and character.
文摘Meizothrombin (MT) is one of prothrombin derivatives which appears in haemostasis activation area. However, its role in haemostasis regulation isn’t clear. We studied the role of MT in fibrin formation, platelet activation and aggregation. A new effective method of obtaining MT from native human prothrombin was developed using immobilised prothrombin activator from Echis multisquamatis venom. The protein was stable and electrophoretically pure. Platelet-rich plasma for aggregation study and gel-sieved platelets for flow-cytometry were separated from blood of healthy donors. It was shown that MT transformed fibrinogen to fibrin and activated clotting factor XIII. MT didn’t activate gel-sieved intact platelets, but in platelet-rich plasma, increased platelet aggregation induced by ADP, collagen and adrenalin.
