Extrinsic Pathway of Blood Coagulation and Thrombin in the Cerebrospinal Fluid after Subarachnoid Hemorrhage

Extrinsic Pathway of Blood Coagulation and Thrombin in the Cerebrospinal Fluid after Subarachnoid... AbstractOBJECTIVE:The involvement of thrombin in the pathophysiology of subarachnoid hemorrhage (SAH) was investigated by comparing thrombin expression and extrinsic pathway activation in the cerebrospinal fluid (CSF) and blood of patients with SAH with the neurological grades, outcome, and presence of delayed cerebral vasospasm.METHODS:Blood and CSF samples were obtained from 38 patients with SAH on Days 3 through 5, 7 through 9, and 12 through 14 after the onset of SAH. CSF samples were also obtained from control patients. Thrombin- antithrombin III complex, prothrombin fragment F1+2, tissue factor, and tissue factor pathway inhibitor were analyzed using enzyme-linked immunosorbent assay.RESULTS:No markers in the blood or CSF were correlated with neurological grades and outcome. Thrombin- antithrombin III complex and prothrombin fragment F1 +2 levels were significantly higher in the CSF of patients with SAH than in the blood or the CSF of control patients and were significantly higher in patients with vasospasm than in patients without vasospasm on Days 7 through 9. Tissue factor levels were significantly higher in the CSF of patients with SAH than in the blood, but the levels were close to those in the CSF of control patients. Tissue factor pathway inhibitor levels in the CSF of patients with SAH and control patients were under the detection limit.CONCLUSION:Thrombin in the blood may not reflect the pathophysiology of SAH. Imbalance between tissue factor and tissue factor pathway inhibitor in the CSF may tend to thrombin generation under normal physiological conditions and also after SAH. Thrombin in the CSF may be involved in the pathophysiology of vasospasm. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurosurgery Oxford University Press

Extrinsic Pathway of Blood Coagulation and Thrombin in the Cerebrospinal Fluid after Subarachnoid Hemorrhage

Extrinsic Pathway of Blood Coagulation and Thrombin in the Cerebrospinal Fluid after Subarachnoid Hemorrhage

CLINICAL STUDIES Extrinsic Pathway of Blood Coagulation and Thrombin in the Cerebrospinal Fluid after Subarachnoid Hemorrhage Michiyasu Suzuki, M .D ., Akira Kudo, M .D ., Yasunari Otawara, M .D., Yutaka Hirashima, M .D ., Akira Takaku, M .D ., Akira Ogawa, M .D. Department of Neurosurgery (MS, AK, Y O , A O ), Iwate Medical University, School of M edicine, Morioka, and Department of Neurosurgery (Y H , AT), Toyam a M edical and Pharmaceutical University, Toyama, )apan OBJECTIVE: The involvement of thrombin in the pathophysiology of subarachnoid hemorrhage (SAH) was investi­ gated by comparing thrombin expression and extrinsic pathway activation in the cerebrospinal fluid (CSF) and blood of patients with SAH with the neurological grades, outcome, and presence of delayed cerebral vasospasm. METHODS: Blood and CSF samples were obtained from 38 patients with SAH on Days 3 through 5, 7 through 9, and 12 through 14 after the onset of SAH. CSF samples were also obtained from control patients. Thrombin- antithrombin III complex, prothrombin fragment F1 + 2 , tissue factor, and tissue factor pathway inhibitor were analyzed using enzyme-linked immunosorbent assay. RESULTS: No markers in the blood or CSF were correlated with neurological grades and outcome. Thrombin- antithrombin III complex and prothrombin fragment F 1 +2 levels were significantly higher in the CSF of patients with SAH than in the blood or the C SF of control patients and were significantly higher in patients with vasospasm than in patients without vasospasm on Days 7 through 9. Tissue factor levels were significantly higher in the CSF of patients with SAH than in the blood, but the levels were close to those in the CSF of control patients. Tissue factor pathway inhibitor levels in the CSF of patients with SAH and control patients were under the detection limit. CONCLUSION: Thrombin in the blood may not reflect the pathophysiology of SAH. Imbalance between tissue factor and tissue factor pathway...
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Publisher
Congress of Neurological Surgeons
Copyright
© Published by Oxford University Press.
ISSN
0148-396X
eISSN
1524-4040
D.O.I.
10.1097/00006123-199903000-00029
Publisher site
See Article on Publisher Site

Abstract

AbstractOBJECTIVE:The involvement of thrombin in the pathophysiology of subarachnoid hemorrhage (SAH) was investigated by comparing thrombin expression and extrinsic pathway activation in the cerebrospinal fluid (CSF) and blood of patients with SAH with the neurological grades, outcome, and presence of delayed cerebral vasospasm.METHODS:Blood and CSF samples were obtained from 38 patients with SAH on Days 3 through 5, 7 through 9, and 12 through 14 after the onset of SAH. CSF samples were also obtained from control patients. Thrombin- antithrombin III complex, prothrombin fragment F1+2, tissue factor, and tissue factor pathway inhibitor were analyzed using enzyme-linked immunosorbent assay.RESULTS:No markers in the blood or CSF were correlated with neurological grades and outcome. Thrombin- antithrombin III complex and prothrombin fragment F1 +2 levels were significantly higher in the CSF of patients with SAH than in the blood or the CSF of control patients and were significantly higher in patients with vasospasm than in patients without vasospasm on Days 7 through 9. Tissue factor levels were significantly higher in the CSF of patients with SAH than in the blood, but the levels were close to those in the CSF of control patients. Tissue factor pathway inhibitor levels in the CSF of patients with SAH and control patients were under the detection limit.CONCLUSION:Thrombin in the blood may not reflect the pathophysiology of SAH. Imbalance between tissue factor and tissue factor pathway inhibitor in the CSF may tend to thrombin generation under normal physiological conditions and also after SAH. Thrombin in the CSF may be involved in the pathophysiology of vasospasm.

Journal

NeurosurgeryOxford University Press

Published: Mar 1, 1999

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