Cerebrospinal Fluid Tissue Factor and Thrombin-Antithrombin III Complex as Indicators of Tissue Injury After Subarachnoid Hemorrhage

Stroke ◽  
1997 ◽  
Vol 28 (9) ◽  
pp. 1666-1670 ◽  
Author(s):  
Yutaka Hirashima ◽  
Shin Nakamura ◽  
Michiyasu Suzuki ◽  
Masanori Kurimoto ◽  
Shunro Endo ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Tissue Factor ◽  
Antithrombin Iii ◽  
Tissue Injury ◽  
Thrombin Antithrombin Iii Complex

Cerebrospinal fluid membrane-bound tissue factor and myelin basic protein in the course of vasospasm after subarachnoid hemorrhage

2001 ◽  
Vol 23 (7) ◽  
pp. 715-720 ◽  
Author(s):  
Yutaka Hirashima ◽  
Shunro Endo ◽  
Shin Nakamura ◽  
Masanori Kurimoto ◽  
Akira Takaku
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Myelin Basic Protein ◽  
Tissue Factor ◽  
Basic Protein ◽  
Fluid Membrane ◽  
Membrane Bound

scholarly journals Subarachnoid hemorrhage – Induced block of cerebrospinal fluid flow: Role of brain coagulation factor III (tissue factor)

2017 ◽  
Vol 38 (5) ◽  
pp. 793-808 ◽  
Author(s):  
Eugene V Golanov ◽  
Evgeniy I Bovshik ◽  
Kelvin K Wong ◽  
Robia G Pautler ◽  
Chase H Foster ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Tissue Factor ◽  
Coagulation Factor ◽  
Csf Flow ◽  
Cerebrospinal Fluid Flow ◽  
Csf Circulation ◽  
New Therapeutic Approaches ◽  
Brain Surface

Subarachnoid hemorrhage (SAH) in 95% of cases results in long-term disabilities due to brain damage, pathogenesis of which remains uncertain. Hindrance of cerebrospinal fluid (CSF) circulation along glymphatic pathways is a possible mechanism interrupting drainage of damaging substances from subarachnoid space and parenchyma. We explored changes in CSF circulation at different time following SAH and possible role of brain tissue factor (TF). Fluorescent solute and fluorescent microspheres injected into cisterna magna were used to track CSF flow in mice. SAH induced by perforation of circle of Willis interrupted CSF flow for up to 30 days. Block of CSF flow did not correlate with the size of hemorrhage. Following SAH, fibrin deposits were observed on the brain surface including areas without visible blood. Block of astroglia-associated TF by intracerebroventricular administration of specific antibodies increased size of hemorrhage, decreased fibrin deposition and facilitated spread of fluorophores in sham/naïve animals. We conclude that brain TF plays an important role in localization of hemorrhage and also regulates CSF flow under normal conditions. Targeting of the TF system will allow developing of new therapeutic approaches to the treatment of SAH and pathologies related to CSF flow such as hydrocephalus.

The Significance of TFPI in Clotting Assays – Gomparison and Combination with other Anticoagulants

1993 ◽  
Vol 70 (03) ◽  
pp. 448-453 ◽  
Author(s):  
Ole Nordfang ◽  
Hanne I Kristensen ◽  
Sanne Valentin ◽  
Per Østergaard ◽  
Johnny Wadt
Keyword(s):  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Antithrombin Iii ◽  
Anticoagulant Activity ◽  
Assay System ◽  
Thrombin Inhibitor ◽  
Clotting Time ◽  
Normal Plasma ◽  
Tissue Factor Pathway ◽  
Plasma Heparin

SummaryThe anticoagulant activities of Tissue Factor Pathway Inhibitor (TFPI), heparin and hirudin were compared in intrinsic (APTT) and extrinsic (PT) activated clotting assays. In contrast to the thrombin inhibitor hirudin, heparin was 10 fold more potent in the APTT assay than in the PT assay, indicating that inhibition of intrinsic activation is important for the anticoagulant activity of heparin as measured in an APTT assay. TFPI was most potent in the PT assay and the effect of TFPI was most pronounced in the presence of other anticoagulants (heparin and hirudin). The activities of the two natural anticoagulants antithrombin III (ATIII) and TFPI were compared in a PT assay with very dilute tissue factor. In this assay system TFPI in normal plasma affected the clotting time more than ATIII in the plasma. However, when heparin was added ATIII was the major anticoagulant, but profound Prolongation of the clotting time was only seen when TFPI was also added. In an ATIII deficient plasma heparin did not augment the effect of TFPI, showing that the increased effect of TFPI in the presence of heparin is dependent on the anticoagulant activity of ATIII/heparin. The effect of TFPI at prolonged clotting times was also illustrated by the significant effect of blocking TFPI in the plasma from warfarin-treated patients. Thus TFPI is a major anticoagulant in normal plasma and the effect of TFPI is especially seen at prolonged clotting times.

scholarly journals Extracellular fluid, cerebrospinal fluid and plasma biomarkers of axonal and neuronal injury following intracerebral hemorrhage

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lovisa Tobieson ◽  
Henrik Zetterberg ◽  
Kaj Blennow ◽  
Niklas Marklund
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracerebral Hemorrhage ◽  
Brain Tissue ◽  
Single Molecule ◽  
Tissue Injury ◽  
Extracellular Fluid ◽  
Neurofilament Light ◽  
Aβ Peptides ◽  
Post Surgery ◽  
Fluid Compartments

AbstractSpontaneous intracerebral hemorrhage (ICH) is the most devastating form of stroke. To refine treatments, improved understanding of the secondary injury processes is needed. We compared energy metabolic, amyloid and neuroaxonal injury biomarkers in extracellular fluid (ECF) from the perihemorrhagic zone (PHZ) and non-injured (NCX) brain tissue, cerebrospinal fluid (CSF) and plasma. Patients (n = 11; age 61 ± 10 years) undergoing ICH surgery received two microdialysis (MD) catheters, one in PHZ, and one in NCX. ECF was analysed at three time intervals within the first 60 h post- surgery, as were CSF and plasma samples. Amyloid-beta (Aβ) 40 and 42, microtubule associated protein tau (tau), and neurofilament-light (NF-L) were analysed using Single molecule array (Simoa) technology. Median biomarker concentrations were lowest in plasma, higher in ECF and highest in CSF. Biomarker levels varied over time, with different dynamics in the three fluid compartments. In the PHZ, ECF levels of Aβ40 were lower, and tau higher when compared to the NCX. Altered levels of Aβ peptides, NF-L and tau may reflect brain tissue injury following ICH surgery. However, the dynamics of biomarker levels in the different fluid compartments should be considered in the study of pathophysiology or biomarkers in ICH patients.

Accelerated Non-Muscle Contraction after Subarachnoid Hemorrhage: Cerebrospinal Fluid Testing in a Culture Model

Neurosurgery ◽  
1990 ◽  
Vol 27 (6) ◽  
pp. 921-928 ◽  
Author(s):  
Yoshihiro Yamamoto ◽  
David H. Bernanke ◽  
Robert R. Smith
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Collagen Matrix ◽  
Aneurysm Rupture ◽  
Lattice Contraction ◽  
Symptomatic Vasospasm ◽  
Luminal Narrowing ◽  
Chronic Vasospasm ◽  
Vitro Model

Abstract The cause of chronic cerebral vasospasm after subarachnoid hemorrhage has been studied intensively, but it is still controversial whether the observable luminal narrowing should be attributed to the contraction of vascular smooth muscle cells or whether it results from some organic change in the wall. A proliferation of myointimal cells, accompanied by increased deposition of collagen, as well as myonecrosis, have been frequently observed several days after aneurysm rupture. Studies from our laboratory showed that these myointimal cells had characteristics identical to myofibroblasts. In this study, we quantitatively and morphologically examined the effect of cerebrospinal fluid on the ability of myofibroblasts to alter collagen matrices using an in vitro model. Myofibroblasts contract the collagen matrix by rearranging or compacting the framework of collagen fibers. Cerebrospinal fluid obtained from patients with recently ruptured aneurysms significantly accelerated lattice contraction, especially when the patient developed symptomatic vasospasm. This study suggests that myofibroblasts in the spastic artery can produce a contractile force that contributes to chronic vasospasm, tightening the proliferated collagen. Some unknown agent present in bloody cerebrospinal fluid accelerates the rearrangement of the collagen lattice by myofibroblasts, both of which have, until now, been considered non-contractile components.

Is there a possible role for haemostasis in the development of perigraft reaction complicating the modified Blalock Taussig shunt?

2000 ◽  
Vol 10 (3) ◽  
pp. 261-264 ◽  
Author(s):  
Ulrike Salzer-Muhar ◽  
Ingrid Pabinger-Fasching ◽  
Sophie Zacherl-Wightman
Keyword(s):  
Antithrombin Iii ◽  
Unusual Complication ◽  
Laboratory Findings ◽  
Thrombin Antithrombin Iii Complex ◽  
Blalock Taussig Shunt

AbstractThe perigraft reaction is an unusual complication found in patients in whom a modified Blalock Taussig shunt has been created using a polytetrafluoroethylene graft. We found that, in two infants, consistent laboratory findings during such a perigraft reaction were hypofibrinogenemia, increased levels of thrombin-antithrombin III complex, prothrombinfragment 1 and 2 and products of degradation of fibrin. Normalization of the levels of fibrinogen produced resolution of the perigraft reaction.

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