The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Zhongchao Han - One of the best experts on this subject based on the ideXlab platform.
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Batroxobin mobilizes circulating endothelial progenitor cells in patients with deep vein thrombosis
Clinical and Applied Thrombosis-Hemostasis, 2011Co-Authors: Lei Zhang, Hirobumi Senga, Yuguo Tao, Yong Ling Wan, Renchi Yang, Zhongchao HanAbstract:Batroxobin, a thrombin-like enzyme from Bothrops atrox moojeni venom, is associated with the reduction of fibrinogen levels in plasma and the enhancement of anticoagulation and fibrinolysis. In this study, 15 patients with deep vein thrombosis (DVT) achieved successful limb salvage after the administration of Batroxobin. We found that the levels of CD34+, CD31+, CD34+/CD31+, and vascular endothelial cadherin (VE-cadherin+) cells had increased in the peripheral blood of patients at 7 days and 14 days after treatment. At 0 day, 7 days, and 14 days, the percentages of CD34+ cells, which are assumed to be hematopoietic stem cells, are 0.39% ± 0.43%, 0.71% ± 0.50%, and 1.11% ± 0.66%, respectively. The levels of CD34+ cells at 14 days are significantly higher than the levels on the first day (P = .004). The levels of CD31+ cells and VE-cadherin+ cells, which represent mature endothelial cells, at 7 days (34.15% ± 11.32%, P = .013; 1.25% ± 1.39%, P = .014) and 14 days (35.21% ± 7.66%, P = .071; 1.85% ± 2.60%, P = .117) were slightly elevated compared with those at 0 day (27.55% ± 8.65%; 0.25 ± 0.39%). The double positive of CD34 and CD31 cells are assumed to be endothelial progenitor cells (EPCs). The levels of CD34+/CD31+ cells at 7 days (0.69% ± 0.50%, P = .001) and 14 days (1.07% ± 0.66%, P = .006) are significantly higher than that on the initial day (0.28% ± 0.30%). The number of CD34+/CD31+ cells significantly increased, indicating that in addition to its role in anticoagulation and fibrinolysis, treatment with Batroxobin might simultaneously activate circulating EPCs that might promote the recanalization of the damaged vessel wall.
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Batroxobin mobilizes circulating endothelial progenitor cells in patients with deep vein thrombosis. Clin
2009Co-Authors: Lei Zhang, Yong Ling Wan, Renchi Yang, Zhongchao HanAbstract:Batroxobin, a thrombin-like enzyme from Bothrops atrox moojeni venom, is associated with the reduction of fibrinogen levels in plasma and the enhancement of anticoagulation and fibrinolysis. In this study, 15 patients with deep vein thrombosis (DVT) achieved successful limb salvage after the administration of Batroxobin. We found that the levels of CD34þ, CD31þ, CD34þ/CD31þ, and vascular endothelial cadherin (VE-cadherinþ) cells had increased in the peripheral blood of patients at 7 days and 14 days after treatment. At 0 day, 7 days, and 14 days, the percentages of CD34þ cells, which are assumed to be hemato-poietic stem cells, are 0.39%+ 0.43%, 0.71%+ 0.50%, and 1.11%+ 0.66%, respectively. The levels of CD34þ cells at 14 days are significantly higher than the levels on the first day (P .004). The levels of CD31þ cells and VE-cadherinþ cells, which rep-resent mature endothelial cells, at 7 days (34.15%+ 11.32%, P .013; 1.25%+ 1.39%, P .014) and 14 days (35.21%+ 7.66%, P .071; 1.85%+ 2.60%, P .117) were slightly elevated compared with those at 0 day (27.55%+ 8.65%; 0.25+ 0.39%). The double positive of CD34 and CD31 cells are assumed to be endothelial progenitor cells (EPCs). The levels of CD34þ/CD31þ cells at 7 days (0.69%+ 0.50%, P .001) and 14 days (1.07%+ 0.66%, P .006) are significantly higher than that on the initial day (0.28%+ 0.30%). The number of CD34þ/CD31þ cells significantly increased, indicating that in addition to its role in antic-oagulation and fibrinolysis, treatment with Batroxobin might simultaneously activate circulating EPCs that might promote the recanalization of the damaged vessel wall
Marcus E. Carr - One of the best experts on this subject based on the ideXlab platform.
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Batroxobin induced clots exhibit delayed and reduced platelet contractile force in some patients with clotting factor deficiencies
Journal of Thrombosis and Haemostasis, 2003Co-Authors: Marcus E. Carr, Sheryl L Carr, T Tildon, Mca L Fisher, Erika J MartinAbstract:Summary. Thrombin causes platelet activation via multiple pathways, and deficient thrombin generation reduces platelet contractile force (PCF) during clot retraction. We hypothesized that PCF in blood samples from clotting factor-deficient patients would be diminished due to delayed or deficient thrombin generation. Blood samples from patients with fibrinogen, and factor V, VII, VIII, IX, X, XI and XIII deficiencies were compared to samples from normal controls. PCF in patient blood clotted with thrombin (1 NIH UmL−1) was compared to PCF in clots formed with Batroxobin (0.25 µg mL−1). PCF in the former should be normal, but PCF in the latter is dependent on thrombin generation within the sample and might be deficient. In factor VII-(n = 2, P < 0.05), factor VIII-(n = 6, P < 0.005) and factor XI-(n = 2, P < 0.05) deficient platelet-rich plasmas, PCF in Batroxobin-induced clots was significantly lower than in thrombin-induced clots. In factor IX deficiency (n = 2), one patient had a dramatic reduction in PCF while a second patient had increased PCF. PCF was insignificantly (P = 0.346) reduced in two patients with factor X deficiency, and was normal in one patient with factor V deficiency. The factor X result is consistent with work in model systems, which indicates that as little as 1–3% factor X activity is sufficient to restore thrombin generation to normal. The factor V result probably indicates that the deficiency is incomplete. PCF in thrombin-induced clots was normal in all of these patients. Low fibrinogen and factor XIII deficiency reduced PCF in both thrombin- and Batroxobin-induced clots. These results indicate that PCF is reduced, probably due to delayed thrombin generation, in some factor-deficient platelet-rich plasma samples.
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delayed reduced or inhibited thrombin production reduces platelet contractile force and results in weaker clot formation
Blood Coagulation & Fibrinolysis, 2002Co-Authors: Marcus E. Carr, Erika J Martin, Sheryl L CarrAbstract:Clot retraction is a thrombin-dependent, platelet-mediated contraction of the cellular clot mass. In this study, the effects of delayed, deficient and inhibited thrombin generation on the development of platelet contractile force (PCF) and clot elastic modulus (CEM) were measured. When normal citrated whole blood is clotted by the addition of exogenous thrombin (1 U/ml) and calcium (10 mmol/l), PCF and CEM start to develop within the first minute and begin to level off by 1200 s. If identical samples are clotted with Batroxobin (0.21 microg/ml) and calcium (10 mmol/l), both PCF and CEM development are delayed approximately 5 min. After 1200 s of clotting, however, values in the Batroxobin system approach those seen with exogenous thrombin. If the added calcium concentration is held constant at 10 mmol/l, increasing the exogenous thrombin concentration from 0 to 0.5 U/ml results in increased PCF and CEM values. Above 0.5 U thrombin, the effect plateaus. At exogenous calcium of 10 mmol/l, increasing Batroxobin concentrations (0-0.210 microg/ml) caused a 75% increase in PCF and a 55% increase in CEM. The increase in CEM reached a plateau above 0.05 microg Batroxobin/ml. The effects of varying calcium concentrations were evaluated at constant Batroxobin (0.21 microg/ml) and thrombin (1 U/ml) concentrations. With thrombin, PCF and CEM increased by > 700% as CaCl2 increased from 0 to 5 mmol/l. Above 5 mmol/l, no additional increases occurred. With Batroxobin, PCF did not develop at CaCl2 concentrations < or = 2.5 mmol/l. Above 2.5 mmol/l CaCl2, PCF values increased and at 10 mmol/l CaCl2 were equal to those seen with thrombin. CEM in Batroxobin-mediated clots peaked at 10 mmol/l CaCl2 but were 40% less than the values found in thrombin-mediated clots. When the thrombin inhibitor P-PACK was added to the Batroxobin system, dose-dependent decreases in PCF and CEM were noted. At 120 micromol/l, P-PACK totally suppressed PCF. PCF in blood from a factor VIII-deficient patient varied significantly when clotted with Batroxobin versus thrombin. PCF development in factor VIII-deficient blood was normal with thrombin but is delayed and depressed with Batroxobin. PCF values in factor VIII-deficient blood did not reach the thrombin value after 1200 s of clotting, and CEM was significantly less. These results confirm that PCF development is thrombin dependent and that delay or reduction of PCF development results in structurally weaker clots.
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heparin ablates force development during platelet mediated clot retraction
Thrombosis and Haemostasis, 1996Co-Authors: Marcus E. Carr, Sheryl L Carr, Philip E GreilichAbstract:: Although snake venom enzymes such as reptilase do not cause viscous metamorphosis, platelet secretion or clot retraction; when Batroxobin and calcium are added to citrated blood significant platelet force development occurs. When this Batroxobin-calcium system was applied to the study of platelet function during cardiopulmonary bypass (CPB), force development was found to be completely inhibited. After heparin reversal by protamine sulfate, significant recovery of force occurred. The present investigation was performed to evaluate the role of heparin in reducing force development during CPB. At concentrations above 0.10 U/ml, heparin totally suppressed force development in normal plasma. Addition of protamine sulfate to heparinized plasma caused complete recovery of force development. These concentrations of heparin had little effect on platelet aggregation by ADP or collagen. Possible direct effects of heparin on fibrin assembly and structure were studied by adding varying amounts of heparin to plasma and then inducing clot formation with Batroxobin. At 1 U/ml, heparin reduced the size of fibrin fibers by 33%. Higher heparin concentrations had no additional effect. These results indicate that heparin may be responsible for a significant component of the decreased platelet force noted during cardiopulmonary bypass. To test whether heparin's effect could be due to suppression of thrombin activity, the effects of the antithrombin hirudin on force development were measured. Hirudin also inhibited force development in a concentration dependent manner. Thus, heparin's reduction of platelet force development may be due, at least in part, to suppression of thrombin activity.
Rajasekeran Shanmuganathan - One of the best experts on this subject based on the ideXlab platform.
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effectiveness and safety of Batroxobin tranexamic acid and a combination in reduction of blood loss in lumbar spinal fusion surgery
Spine, 2018Co-Authors: Roopa M Nagabhushan, Ajoy Prasad Shetty, Srikanth Reddy Dumpa, Balavenkat Subramanian, Rishi Mugesh Kanna, Rajasekeran ShanmuganathanAbstract:STUDY DESIGN A prospective randomized double blind placebo controlled trail. OBJECTIVE To evaluate and compare the efficacy and safety of Batroxobin (botropase), tranexamic acid (TXA), and their combination in reduction of perioperative blood loss in lumbar spine single level fusion surgeries. SUMMARY OF BACKGROUND DATA Spinal surgeries are associated with significant blood loss leading to perioperative anemia and increased need for allogenic transfusion. TXA competitively inhibits plasmin and Batroxobin converts fibrinogen to fibrin and theoretically their combination is synergistic. Though TXA is widely studied in controlling blood loss, there is little information on use of Batroxobin and their combination. Thus, we aimed to study effect and safety of individual drugs and their combination in controlling blood loss in spinal surgery. METHODS Hundred patients were randomized into four groups. Group B received Batroxobin, group T received TXA, group BT received Batroxobin and TXA and group P received placebo. Outcomes assessed are intraoperative and postoperative blood loss, hematocrit, allogenic blood transfusion, and deep vein thrombosis (DVT), postoperatively. RESULT Mean intraoperative blood loss in Group B, T, BT, and P were 268.32 ± 62.92 mL, 340.72 ± 182.75 mL, 256.96 ± 82.64 mL, and 448.44 ± 205.86 mL, respectively. Postoperative surgical site drain collection in Group B, T, BT, and P were 218.00 ± 100.54 mL, 260.40 ± 100.85 mL, 191.00 ± 87.84 mL, and 320.00 ± 125.83 mL, respectively. Intraoperative blood loss of Group P was statistically higher than Groups B and BT (P < 0.001). Mean postoperative surgical site drain collection was statistically significant (P < 0.001). No statistically significant differences in fluid administration (P = 0.751), blood transfusion (P = 1.000), preoperative and postoperative hemoglobin (P = 0.090, P = 0.134, respectively), and deep vein thrombosis (P = 1.000). CONCLUSION Batroxobin and combination of Batroxobin with tranexamic acid significantly reduced perioperative blood loss when compared with placebo. LEVEL OF EVIDENCE 2.
Yazhou Wang - One of the best experts on this subject based on the ideXlab platform.
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protective effects of Batroxobin on spinal cord injury in rats
Neuroscience Bulletin, 2013Co-Authors: Hong Fan, Xia Liu, Haibin Tang, Peng Xiao, Yazhou WangAbstract:Expansion of the secondary injury following primary spinal cord injury is a major pathological event that increases destruction in the spinal cord, so measures to reduce secondary injury are needed. Our previous study demonstrated that, at the front of the expanding secondary injury in the spinal cord, there is an ischemic area in which many neurons can still be rescued. Therefore, enhancement of blood circulation in the cord may be helpful, and indeed, we found that a traditional Chinese medicine, shu-xue-tong, efficiently reduces the secondary injury. The aim of the present study was to investigate the effect of reducing fibrinogen with Batroxobin, a drug widely used clinically for ischemia, in rats with spinal cord contusion. We found that both 2 and 4 Batroxobin units (BU)/kg efficiently decreased the plasma fibrinogen, and 2 BU/kg significantly increased spinal blood flow, enhanced neuronal survival, mitigated astrocyte and microglia activation, and improved locomotor recovery. However, 4 BU/kg had no effect on the secondary spinal cord injury. These data suggest that Batroxobin has multiple beneficial effects on spinal cord injury, indicating a potential clinical application.
Erika J Martin - One of the best experts on this subject based on the ideXlab platform.
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Batroxobin induced clots exhibit delayed and reduced platelet contractile force in some patients with clotting factor deficiencies
Journal of Thrombosis and Haemostasis, 2003Co-Authors: Marcus E. Carr, Sheryl L Carr, T Tildon, Mca L Fisher, Erika J MartinAbstract:Summary. Thrombin causes platelet activation via multiple pathways, and deficient thrombin generation reduces platelet contractile force (PCF) during clot retraction. We hypothesized that PCF in blood samples from clotting factor-deficient patients would be diminished due to delayed or deficient thrombin generation. Blood samples from patients with fibrinogen, and factor V, VII, VIII, IX, X, XI and XIII deficiencies were compared to samples from normal controls. PCF in patient blood clotted with thrombin (1 NIH UmL−1) was compared to PCF in clots formed with Batroxobin (0.25 µg mL−1). PCF in the former should be normal, but PCF in the latter is dependent on thrombin generation within the sample and might be deficient. In factor VII-(n = 2, P < 0.05), factor VIII-(n = 6, P < 0.005) and factor XI-(n = 2, P < 0.05) deficient platelet-rich plasmas, PCF in Batroxobin-induced clots was significantly lower than in thrombin-induced clots. In factor IX deficiency (n = 2), one patient had a dramatic reduction in PCF while a second patient had increased PCF. PCF was insignificantly (P = 0.346) reduced in two patients with factor X deficiency, and was normal in one patient with factor V deficiency. The factor X result is consistent with work in model systems, which indicates that as little as 1–3% factor X activity is sufficient to restore thrombin generation to normal. The factor V result probably indicates that the deficiency is incomplete. PCF in thrombin-induced clots was normal in all of these patients. Low fibrinogen and factor XIII deficiency reduced PCF in both thrombin- and Batroxobin-induced clots. These results indicate that PCF is reduced, probably due to delayed thrombin generation, in some factor-deficient platelet-rich plasma samples.
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delayed reduced or inhibited thrombin production reduces platelet contractile force and results in weaker clot formation
Blood Coagulation & Fibrinolysis, 2002Co-Authors: Marcus E. Carr, Erika J Martin, Sheryl L CarrAbstract:Clot retraction is a thrombin-dependent, platelet-mediated contraction of the cellular clot mass. In this study, the effects of delayed, deficient and inhibited thrombin generation on the development of platelet contractile force (PCF) and clot elastic modulus (CEM) were measured. When normal citrated whole blood is clotted by the addition of exogenous thrombin (1 U/ml) and calcium (10 mmol/l), PCF and CEM start to develop within the first minute and begin to level off by 1200 s. If identical samples are clotted with Batroxobin (0.21 microg/ml) and calcium (10 mmol/l), both PCF and CEM development are delayed approximately 5 min. After 1200 s of clotting, however, values in the Batroxobin system approach those seen with exogenous thrombin. If the added calcium concentration is held constant at 10 mmol/l, increasing the exogenous thrombin concentration from 0 to 0.5 U/ml results in increased PCF and CEM values. Above 0.5 U thrombin, the effect plateaus. At exogenous calcium of 10 mmol/l, increasing Batroxobin concentrations (0-0.210 microg/ml) caused a 75% increase in PCF and a 55% increase in CEM. The increase in CEM reached a plateau above 0.05 microg Batroxobin/ml. The effects of varying calcium concentrations were evaluated at constant Batroxobin (0.21 microg/ml) and thrombin (1 U/ml) concentrations. With thrombin, PCF and CEM increased by > 700% as CaCl2 increased from 0 to 5 mmol/l. Above 5 mmol/l, no additional increases occurred. With Batroxobin, PCF did not develop at CaCl2 concentrations < or = 2.5 mmol/l. Above 2.5 mmol/l CaCl2, PCF values increased and at 10 mmol/l CaCl2 were equal to those seen with thrombin. CEM in Batroxobin-mediated clots peaked at 10 mmol/l CaCl2 but were 40% less than the values found in thrombin-mediated clots. When the thrombin inhibitor P-PACK was added to the Batroxobin system, dose-dependent decreases in PCF and CEM were noted. At 120 micromol/l, P-PACK totally suppressed PCF. PCF in blood from a factor VIII-deficient patient varied significantly when clotted with Batroxobin versus thrombin. PCF development in factor VIII-deficient blood was normal with thrombin but is delayed and depressed with Batroxobin. PCF values in factor VIII-deficient blood did not reach the thrombin value after 1200 s of clotting, and CEM was significantly less. These results confirm that PCF development is thrombin dependent and that delay or reduction of PCF development results in structurally weaker clots.
