Increase in brain thrombin activity after experimental intracerebral hemorrhage

2009 ◽  
pp. 47-50 ◽  
Author(s):  
Y. Gong ◽  
G. Xi ◽  
H. Hu ◽  
Y. Gu ◽  
F. Huang ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Thrombin Activity

The Role of Stereotactic Technology in the Management of Intracerebral Hemorrhage

1992 ◽  
Vol 3 (3) ◽  
pp. 685-702 ◽  
Author(s):  
Christopher B. Shields ◽  
William A. Friedman
Keyword(s):  
Intracerebral Hemorrhage

Erythropoietin induces neuroprotection in experimental intracerebral hemorrhage via eNOS upregulation and STAT3 activation

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S481-S481
Author(s):  
Soon-Tae Lee ◽  
Kon Chu ◽  
Manho Kim ◽  
Jae-kyu Roh
Keyword(s):  
Intracerebral Hemorrhage

Neuroprotective effect of antisense oligodeoxynucleotides in experimental intracerebral hemorrhage in rats

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S505-S505
Author(s):  
Huijin Yan ◽  
Mengzhou Xue ◽  
Christopher Power ◽  
Marc R Del-Bigio ◽  
James Peeling
Keyword(s):  
Intracerebral Hemorrhage ◽  
Neuroprotective Effect ◽  
Antisense Oligodeoxynucleotides

Radiolabeled r-Hirudin as a Measure of Thrombin Activity at, or within, the Rabbit Aorta Wall In Vitro and In Vivo

1994 ◽  
Vol 71 (04) ◽  
pp. 499-506 ◽  
Author(s):  
Mark W C Hatton ◽  
Bonnie Ross-Ouellet
Keyword(s):  
Rabbit Aorta ◽  
Balloon Injury ◽  
Recombinant Hirudin ◽  
Aorta Wall ◽  
Thrombin Activity ◽  
Before And After ◽  
The Matrix

SummaryThe behavior of 125I-labeled recombinant hirudin towards the uninjured and de-endothelialized rabbit aorta wall has been studied in vitro and in vivo to determine its usefulness as an indicator of thrombin activity associated with the aorta wall. Thrombin adsorbed to either sulfopropyl-Sephadex or heparin-Sepharose bound >95% of 125I-r-hirudin and the complex remained bound to the matrix. Binding of 125I-r-hirudin to the exposed aorta subendothelium (intima-media) in vitro was increased substantially if the tissue was pre-treated with thrombin; the quantity of l25I-r-hirudin bound to the de-endothelialized intima-media (i.e. balloon-injured in vitro) correlated positively with the quantity of bound 131I-thrombin (p <0.01). Aortas balloon-injured in vivo were measured for thrombin release from, and binding of 125I-r-hirudin to, the de-endothelialized intimal surface in vitro; 125I-r-hirudin binding correlated with the amount of active thrombin released (p <0.001). Uptake of 125I-r-hirudin by the aorta wall in vivo was proportional to the uptake of 131I-fibrinogen (as an indicator of thrombin activity) before and after balloon injury. After 30 min in the circulation, specific 125I-r-hirudin binding to the uninjured and de-endo- thelialized (at 1.5 h after injury) aorta wall was equivalent to 3.4 (± 2.5) and 25.6 (±18.1) fmol of thrombin/cm2 of intima-media, respectively. Possibly, only hirudin-accessible, glycosaminoglycan-bound thrombin is measured in this way.

Potato Inhibitors of Intrinsic Prothrombin Activators

1975 ◽  
Vol 34 (03) ◽  
pp. 763-769
Author(s):  
K Worowski
Keyword(s):  
Protease Inhibitors ◽  
No Inhibition ◽  
Thrombin Activity ◽  
Tissue Thromboplastin

SummaryThe potato protease inhibitors inhibit intrinsic prothrombin activators and trypsin activation of prothrombin. The inhibitors 5a and 5b are responsible for the intrinsic prothrombin activator inhibition. This inhibition is progressive. No inhibition by these inhibitors of tissue thromboplastin activation of prothrombin or thrombin activity was observed.

The Ability of Thrombin Inhibitors to Reduce the Thrombin Activity Generated in Plasma on Extrinsic and Intrinsic Activation

1997 ◽  
Vol 77 (03) ◽  
pp. 498-503 ◽  
Author(s):  
D Prasa ◽  
L Svendsen ◽  
J Stürzebecher
Keyword(s):  
Active Site ◽  
Thrombin Generation ◽  
Anion Binding ◽  
Thrombin Inhibitors ◽  
Coagulation System ◽  
Thrombin Activity ◽  
Continuous Registration ◽  
High Concentrations ◽  
20 Nm ◽  
Generation Test

SummaryIn a thrombin generation test with continuous registration of thrombin activity in plasma we studied the ability of a variety of thrombin inhibitors of different type and mechanism of action to influence the activity of thrombin after activation of the coagulation system. Depending on the inhibitor, the peak of thrombin activity is delayed and/or reduced.By blocking the active site of generated thrombin inhibitors cause a concentration dependent reduction of the thrombin peak and inhibit feed-back reactions of thrombin resulting in a delay of thrombin generation. Highly potent synthetic active-site directed inhibitors (Ki ≤ 20 nM) reduce the thrombin activity formed in plasma after extrinsic or intrinsic activation with the same efficiency (IC50 0.1 - 0.6 μM) as hirudin. The delay and reduction of thrombin generation by inhibitors of the anion-binding exosite 1 of thrombin is only attributed to an inhibition of feed-back reactions of thrombin. For a 50% reduction of thrombin activity in plasma by this type of inhibitors relatively high concentrations were determined.

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