1.Research Progress of Carboxymethyl Chitosan-Based Haemostatic Materials and Their Haemostatic Mechanism --Review.
Kang REN ; Li-Hao WU ; Ling XU
Journal of Experimental Hematology 2023;31(3):911-915
Effective haemostatic materials can quickly control bleeding and achieve the purpose of saving patients' lives. In recent years, chitosan-based haemostatic materials have shown good haemostatic effects, but their application is limited because chitosan is almost insoluble in water. Carboxymethyl chitosan-based haemostatic materials can promote hemostasis by activating red blood cells and aggregating platelets. In addition, carboxymethyl chitosan can bind with Ca2+ to activate platelets and coagulation factors, and start endogenous coagulation pathways, which can adsorb fibrinogen in plasma to promote haemostasis. In this paper, the latest research progress of carboxymethyl chitosan-based haemostatic materials and their haemostatic mechanism were reviewed, in order to further strengthen the understanding of the haemostatic mechanism of carboxymethyl chitosan-based haemostatic materials, and provide new idea for the research and clinical application of carboxymethyl chitosan-based haemostatic materials.
Humans
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Hemostatics
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Chitosan/pharmacology*
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Hemostasis
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Blood Coagulation/physiology*
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Hemorrhage
2.Cryopreservation strengthens procoagulative activities of platelets.
Xi-Lin OUYANG ; Dan ZHOU ; Jing-Hui WU ; Li-Hua WANG ; Jun HAO ; Jing-Han LIU
Journal of Experimental Hematology 2008;16(4):930-932
The aim of this study was to explore the potential relationship between the enhancement of instant hemostatic function in vivo of cryopreserved platelets and its procoagulative related molecule activities. The ability of platelet binding factor V density of GPIb-IX-V (CD42a) at platelet member surface were detected by flow cytometry, the clotting time induced by activated platelets were evaluated by coagulometer and platelet count, MPV and PDW were measured by hemocytometer before and after fresh platelets were cryopreserved. The results showed that the clotting time induced by activated cryopreserved platelets decreased by 43.9%, even quicker than that induced by fresh platelets; the fluorescence intensity of cryopreserved platelet binding factor V increased by 117%, more than that of fresh platelets binding factor V; the GPIb-IX-V (CD42a) density at cryopreserved platelet membrane surface increased by 32%, higher than that at fresh platelet surface. It is concluded that the enhancement of instant hemostatic function in vivo of cryopreserved platelet may be related to higher expression of procoagulative molecules or to their enhanced activity and rapid hemostatic effect.
Blood Coagulation
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physiology
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Blood Coagulation Factors
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metabolism
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Blood Platelets
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physiology
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Blood Preservation
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Cryopreservation
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methods
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Humans
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Platelet Glycoprotein GPIb-IX Complex
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analysis
3.Orthostatic Intolerance and Coagulation Abnormalities: An Update.
Wei QUAN ; Yuchen WANG ; Selena CHEN ; Junbao DU
Neuroscience Bulletin 2019;35(1):171-177
4.Expression and procoagulant activity of phosphatidylserine on the normal blood cells.
Shu-chuan LIU ; Jin ZHOU ; Jia-lan SHI ; Yan-hua SU
Chinese Journal of Hematology 2011;32(12):858-862
OBJECTIVETo investigate the expression and procoagulant activity of phosphatidylserine (PS) on the normal peripheral blood cells of adults.
METHODSNormal peripheral blood samples were collected from 10 healthy volunteers (5 ml from each volunteer), platelets, neutrophils, lymphocytes and erythrocytes were isolated. The expression and procoagulant activity of PS on normal blood cells were identified by flow cytometry, inhibition test with lactadherin as PS probe and coagulation anticoagulant, respectively.
RESULTSThere was PS expression on a few normal blood cells (9.1%, 5.4%, 3.9% and 3.2% in platelets, neutrophils, lymphocytes and erythrocytes, respectively). The PS on these normal blood cells in vitro showed significant procoagulant activity. The plasma recalcification time was shortened by 47%, 36.5%, 25% and 12.5% by platelets, neutrophils, lymphocytes and erythrocytes, respectively; the formation of factor Xa (through both intrinsic and extrinsic pathways) and thrombin was also increased by 13% - 26% by platelets, neutrophils, lymphocytes and erythrocytes, respectively.
CONCLUSIONThe PS on normal blood cells in vivo may play a crucial role in the coagulation cascade.
Adult ; Blood Cells ; metabolism ; physiology ; Blood Coagulation Tests ; Female ; Flow Cytometry ; Humans ; Male ; Phosphatidylserines ; metabolism
6.Effects of chronic mercury poisoning on blood coagulation and fibrinolysis systems.
Chinese Journal of Industrial Hygiene and Occupational Diseases 2005;23(6):405-407
OBJECTIVETo investigate the effects of chronic mercury poisoning on blood coagulation and fibrinolysis systems, and the possible mechanism.
METHODSTwenty-seven patients with chronic mercury poisoning were studied with 30 healthy people as control. Thrombomodulin (TM), tissue plasminogen activator (t-PA), plasminogen activator inhibitor (PAI), interleukin-13 (IL-13), interleukin-18 (IL-18), soluble intercellular adhesion molecule-1 (SICAM-1) were examined with ELISA methods, and superoxide dismutase (SOD) and lipid peroxidation (LPO) was examined with chemical catalysis methods. Two to three weeks after treatment with reduced glutathione, tiopronin and daidzein, blood was used for determin the above items again.
RESULTS(1) The concentration of TM in patients [(2.36 +/- 0.16) ng/ml] was significantly lower than in the control [(4.36 +/- 0.24) ng/ml] (P < 0.01), while TM tended to be higher after treatment [(4.82 +/- 0.34) ng/ml] (P < 0.05). (2) The concentration of t-PA in patients [(3.44 +/- 0.34) ng/ml] was significantly lower than in the control [(4.52 +/- 0.16) ng/ml] (P < 0.05), and was higher significantly [(5.63 +/- 0.58) ng/ml] after treatment (P < 0.05); The concentration of PAI in patients [(48.23 +/- 3.59) ng/ml] was significantly higher than in the control [(31.59 +/- 2.13) ng/ml] (P < 0.05), but after treatment no significant change [(50.71 +/- 4.29) ng/ml] was found (P > 0.05). (3) The activity of SOD in patients [(953.85 +/- 9.56) U/g Hb] was significantly lower than in the control [(1,308.75 +/- 10.21) U/g Hb] (P < 0.01), and was higher significantly [(1,217.95 +/- 6.29) U/g Hb] after treatment (P < 0.05); and the concentration of LPO in patients [(9.53 +/- 0.26) nmol/ml] was significantly higher than in the control (P < 0.05), and significantly lower [(7.29 +/- 0.35) nmol/ml] after treatment (P < 0.05). (4) The concentrations of IL-13 [(35.93 +/- 5.28) pg/ml], IL-18 [(28.79 +/- 2.53) pg/ml], SICAM-1 [(603.16 +/- 29.12) ng/ml] were significantly higher than those in the controls (P < 0.05, P < 0.01), but no significant difference was found after treatment.
CONCLUSIONDysfunction of the TM/protein C system and t-PA/PAI system (i.e. the decrease of anti-coagulation activity and the inhibition of the function for the fibrolysis system) may play a key role in the secondary hypercoagulable state induced by chronic mercury poisoning.
Adult ; Blood Coagulation ; physiology ; Case-Control Studies ; Chronic Disease ; Female ; Fibrinolysis ; physiology ; Humans ; Male ; Mercury Poisoning ; blood ; physiopathology ; Plasminogen Inactivators ; blood ; Thrombomodulin ; blood ; Tissue Plasminogen Activator ; blood
7.Research progress of acute coagulopathy of trauma-shock.
Chinese Journal of Traumatology 2015;18(2):95-97
Acute coagulopathy of trauma-shock (ACoTS) occurs in 25% of patients with severe trauma in the early phase, and the mortality of those patients is four-fold higher than patients without coagulopathy. The pathophysiology of this complicated phenomenon has been focused on in recent years. Tissue injury and hypoperfusion, activated protein C and Complements play important roles in the early phase after trauma. While the use of blood products, hypothermia, acidosis and inflammation are the main mechanism in late phase. Supplementing coagulation factors and platelets to improve ACoTS are inefficient. Only positive resuscitation from shock and improving tissue hypoperfusion have expected benefits.
Blood Coagulation Disorders
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etiology
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Complement System Proteins
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physiology
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Disseminated Intravascular Coagulation
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etiology
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Humans
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Hypothermia
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complications
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Inflammation
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complications
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Protein C
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physiology
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Shock, Traumatic
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complications
8.Clinical and biological analysis in graftless maxillary sinus lift.
Marcelo PARRA ; Sergio OLATE ; Mario CANTÍN
Journal of the Korean Association of Oral and Maxillofacial Surgeons 2017;43(4):214-220
Maxillary sinus lift for dental implant installation is a well-known and versatile technique; new techniques are presented based on the physiology of intrasinus bone repair. The aim of this review was to determine the status of graftless maxillary sinus lift and analyze its foundations and results. A search was conducted of the literature between 1995 and 2015 in the Medline, ScienceDirect, and SciELO databases using the keywords “maxillary sinus lift,”“blood clot,”“graftless maxillary sinus augmentation,” and “dental implant placement.” Ten articles were selected for our analysis of this technique and its results. Despite the limited information, cases that were followed for at least six months and up to four years had a 90% success rate. Published techniques included a lateral window, elevation of the sinus membrane, drilling and dental implant installation, descent of the membrane with variations in the installation of the lateral wall access and suturing. The physiology behind this new bone formation response and the results of the present research were also discussed. We concluded that this is a promising and viable technique under certain inclusion criteria.
Blood Coagulation
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Dental Implants
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Foundations
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Maxillary Sinus*
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Membranes
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Osteogenesis
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Physiology
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Sinus Floor Augmentation
9.The effect of hepatic blood inflow occlusion on hepatic cancer treated with diode-laser thermocoagulation.
De-fei HONG ; Song-ying LI ; Li-min TONG ; Bin CHEN ; Shu-you PENG
Journal of Zhejiang University. Science. B 2005;6(4):232-235
OBJECTIVETo assess the effect of temporary occlusion of hepatic blood inflow on hepatic cancer treated with diode-laser induced thermocogation (LITT).
METHODSThe carcinoma Walker-256 was implanted in 40 SD rat livers. Twelve days later, the animals were randomly divided into 4 groups. Group A received LITT alone; group B received hepatic artery temporary occlusion during LITT; group C received portal vein temporary occlusion during LITT; group D received hepatic artery and portal vein temporary occlusion during LITT. Tumors were exposed to 810 nm diode-laser light at 0.95 watts for 10 min from a scanner tip applicator placed in the tumor. At the same time, the intrahepatic temperature distribution in rats with liver tumors was measured per 2 min during thermocoagulation. Tumor control was examined immediately 7 and 14 d after thermocoagulation.
RESULTSThere was significant difference of intrahepatic temperature distribution in rats with liver tumors among the 4 groups (P<0.05) except when group C samples were compared with group D samples at each time point, and group B samples were compared with group C samples at 120 s (P>0.05). Light microscopic examination of the histologic section samples revealed three separate zones: regular hyperthermic coagulation necrosis zone, transition zone and reference zone. Compared with the samples in group A and group B, group C and group D samples had more clear margin among the three zones.
CONCLUSIONThe hepatic blood inflow occlusion, especially portal vein hepatic blood inflow occlusion, or all hepatic blood inflow occlusion considerably increased the efficacy of LITT in the treatment of liver cancer.
Animals ; Laser Coagulation ; Liver Circulation ; physiology ; Liver Neoplasms ; blood supply ; surgery ; Rats ; Temperature ; Time Factors
10.Increased procoagulant activity of red blood cells in the presence of cisplatin.
Cheng-fang LÜ ; Hong-juan YU ; Jin-xiao HOU ; Jin ZHOU
Chinese Medical Journal 2008;121(18):1775-1780
BACKGROUNDCisplatin based chemotherapy is a well recognized risk factor for coagulation disorders and thrombosis. The pathophysiological mechanisms by which cisplatin promote thrombosis are not well understood.
METHODSRed blood cells (RBCs) were separated from peripheral blood of patients with breast cancer (n = 10) and healthy adults (n = 6) and treated with cisplatin. Coagulation time of RBCs was assessed by one step recalcification time and the productions of thrombin, intrinsic and extrinsic factor Xa were measured in the presence or absence of various concentrations of lactadherin. Exposed phosphatidylserine was stained with lactadherin and observed by confocal microscopy and flow cytometry.
RESULTSNeither fresh RBCs nor RBCs treated without cisplatin had potent procoagulant activity. Cisplatin treatment increased procoagulant activity of RBCs in a cell number- and concentration-dependent manner. Exposed phosphatidylserine was stained with lactadherin and after cisplatin treatment, strong fluorescence was revealed by confocal microscopy. Lactadherin bound RBCs from patients with breast cancer increased from (1.9 +/- 0.5)% on control RBCs to (68.0 +/- 3.5)% on RBCs treated with 10 micromol/L cisplatin for 24 hours.
CONCLUSIONSCisplatin treatment increases procoagulant activity of RBCs, which have a strong association with exposure of phosphatidylserine. The increased procoagulant activity may contribute to the pathogenesis of thrombophilia during cisplatin based chemotherapy in breast cancer patients.
Antineoplastic Agents ; pharmacology ; Blood Coagulation ; drug effects ; physiology ; Cisplatin ; pharmacology ; Erythrocytes ; drug effects ; physiology ; Humans ; In Vitro Techniques