الفهرس 
Physiology of HemostasisOnly 14 pages are availabe for public view
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Abstract
The normal hemostatic response to vascular damage depends on closely linked interaction between the blood vessel wall, circulating platelets and blood coagulation factors. Coagulation begins almost after an injury to the blood vessel that damaged the endothelial lining of the vessel. Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously when plasma proteins, (coagulation factors) respond in a complex cascade to form fibrin strands, which strengthen the platelet plug..
Soluble platelet-selectin (sP-selectin) is an indicator of platelet activation, fibrinogen (FIB) level is a reflection of clotting ability in the body, and Von Willebrand factor (vWF) is essential for normal thrombus formation..
Antithrombin (AT) rapidly neutralizes the thrombin generated to form inactive thrombin-antithrombin complex (TAT) which is a sensitive marker of activation of coagulation and thrombin generation. Protein C is a major physiological anticoagulant which acts with its cofactor protein S to inactivate factor Va and factor VIIIa.
When a clot is formed, plasminogen changes into plasmin which degrades fibrinogen and fibrin to produce fibrin degradation products (FDPs) D-dimer and respectively. D-dimer is the final product of the simultaneous activation of blood coagulation and fibrinolysis. There is an extensive cross-talk between inflammation and coagulation where the proinflammatory cytokines (IL-1β, IL-6 and TNF-α) appear during the inflammatory states and establish a procoagulant shift in the hemostatic balance, promoting fibrin generation.
This randomized study was conducted from January 2017 till January 2018. It was designed to assess the changes of routine screening coagulation tests (namely; PT, PC, PTT, INR and platelet count) , specific coagulation parameters (namely; fibrinogen, vWF and TAT complex), anticoagulant proteins (namely; AT, protein C and protein S), fibrinolysis protein (plasminogen) and simultaneous coagulation and fibrinolytic parameter (D-dimer) and inflammatory markers (hs CRP, IL-1β and IL-6) in patients undergoing either laparoscopic or open cholecystectomy under the effect of sevoflurane versus isoflurane inhalational agents.
These parameters were assessed at the following timings; preoperative (baseline), immediate post-operative and 24 hours after surgery.
vWF was elevated postoperatively in all groups but with higher level in the open cholecystectomy (OC) group and anaesthetized with Isoflurane than the laparoscopic cholecystectomy (LC) group and anaesthetized with Sevoflurane.
The highest levels of Fibrinogen plasma levels were observed in the IO group and the lowest levels were in the SL group. The highest levels of TAT complex were observed in the IO group and the lowest levels were in the SL.
Plasmin splits the cross-linked fibrin to produce D-dimer. D-dimer level was significantly higher in OC anaesthetized with Isoflurane than in LC anaesthetized with Sevoflurane.
The cytokine surge was associated with hypercoagulability. The lack of significant hypercoagulability in LC correlates with the moderate increase in serum cytokine level. In contrast, in the OC group when IL- 6 and IL-1 β levels were markedly elevated, cytokine levels were associated with more hypercoagulability, as suggested especially by increase fibrinogen, vWF and TAT complex. The highest levels of IL- 6 and IL-1 β were observed in the IO group and the lowest levels were in SL group.