Acute Local Fibrinolysis for Embolic Middle Cerebral Artery Occlusion Using Recombinant Tissue Type Plasminogen Activator

1995 ◽  
pp. 335-338 ◽  
Author(s):  
M. Ezura ◽  
A. Takahashi ◽  
T. Yoshimoto
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Plasminogen Activator ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Local Fibrinolysis ◽  
Cerebral Artery Occlusion

scholarly journals Tissue-Type Plasminogen Activator has Paradoxical Roles in Focal Cerebral Ischemic Injury by Thrombotic Middle Cerebral Artery Occlusion with Mild or Severe Photochemical Damage in Mice

2002 ◽  
Vol 22 (6) ◽  
pp. 648-651 ◽  
Author(s):  
Nobuo Nagai ◽  
Bing-Qiao Zhao ◽  
Yasuhiro Suzuki ◽  
Hayato Ihara ◽  
Tetsumei Urano ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Tissue Type ◽  
Severe Damage ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Photochemical Damage ◽  
Cerebral Ischemic ◽  
Cerebral Artery Occlusion

The role of endogenous tissue-type plasminogen activator (tPA) in focal cerebral ischemic injury (FCII) after middle cerebral artery occlusion was studied using tPA gene-deficient (KO) mice and their wild-type (WT) littermates. The middle cerebral artery was occluded by thrombi induced by three different intensities of photochemical damage, a method that was newly introduced in mice. In both WT and KO mice, the intensity-dependent increase of FCII size was observed. The FCII size in tPA WT mice was smaller than in KO mice in cases of mild damage, whereas the FCII size was larger in WT mice than in KO mice in cases of severe damage. There was no difference in FCII size between WT and KO mice in cases of moderate damage. The number of microthrombi also increased with damage intensity in both WT and KO mice, but was less in WT mice at all intensities of damage. The results support the validity of the model of thrombotic occlusion by photochemical damage in mice, and suggest that endogenous tPA protects FCII through thrombolytic action on transient occlusion of middle cerebral artery with mild damage, but deteriorates on persistent occlusion with severe damage.

Abstract 1029: Stromelysin-1 is Critical For Intracranial Bleeding After Tissue-type plasminogen activator Treatment Of Stroke In Mice

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Yasuhiro Suzuki ◽  
Nobuo Nagai ◽  
Desire Collen ◽  
Roger Lijnen ◽  
Kazuo Umemura
Keyword(s):  
Ischemic Stroke ◽  
Plasminogen Activator ◽  
Placebo Treatment ◽  
Artery Occlusion ◽  
Intracranial Bleeding ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Mmp Inhibitor ◽  
Type Plasminogen Activator ◽  
Cerebral Artery Occlusion

Background: Tissue-type plasminogen activator (t-PA) is approved for treatment of ischemic stroke patients, but it may increase the risk of intracranial bleeding (ICB). Matrix metalloproteinases (MMPs), which can be activated through the plasminogen/plasmin system, may contribute to ICB after ischemic stroke. Objectives: To explore the contribution of plasminogen, MMP-3 and MMP-9 to ICB associated with t-PA treatment after ischemic stroke. Methods: Using a thrombotic middle cerebral artery occlusion (MCA-O) model, ICB was studied in mice with genetic deficiencies of plasminogen (Plg −/ − ), stromelysin-1 (MMP-3 −/ − ) or gelatinase B (MMP-9 −/ − ) and their corresponding wild-type (WT) littermates. t-PA (10 mg/kg) or its equivalent volume of solvent was administered intravenously 4 hours after MCA-O. The induction of MMP-3 and MMP-9 was also studied in C57BL/6 WT mice. Results: In MMP-3 +/+ WT mice given solvent, ICB was 4.3 ± 2.9 mm 3 (mean ± SD), which was significantly increased with tPA treatment to 9.7 ± 4.7 mm 3 (P<0.05), whereas ICB in MMP-3 −/ − mice was not altered by t-PA treatment (5.7 ± 2.7 mm 3 , as compared to 5.1 ± 1.8 mm 3 without tPA; n = 7–9 in each group). ICB induced by t-PA was significantly less in Plg −/ − (5.7 ± 3.9 mm 3 ) than in WT mice (8.8 ± 3.2 mm 3 , p<0.05) but ICB by t-PA in MMP-9 −/ − (8.3 ± 2.3 mm 3 ) was comparable with that in WT (8.3 ± 3.1 mm 3 ; n=8 –12 in each group). Administration of the broad-spectrum MMP inhibitor GM6001 after t-PA treatment reduced ICB significantly in MMP-3 +/+ (from 6.4 ± 1.9 mm 3 to 4.1 ± 1.9 mm 3 , p<0.05) but not in MMP-3 −/ − mice (2.2 ± 0.6 mm 3 without versus 2.9 ± 1.5 mm 3 with GM6001; n=6 – 8 in each group). MMP-3 expression was significantly enhanced at the ischemic hemisphere; with placebo treatment, it was expressed only in neurons, whereas it was upregulated in endothelial cells with t-PA treatment. Although MMP-9 expression was also significantly enhanced at the ischemic brain, the amount and the distribution were comparable in mice with and without t-PA treatment. Conclusions: Our data with gene deficient mice suggest that plasminogen and MMP-3 are relatively more important than MMP-9 for the increased ICB induced by t-PA treatment of ischemic stroke.

Increased expression of tissue-type transglutaminase following middle cerebral artery occlusion in rats

2004 ◽  
Vol 89 (5) ◽  
pp. 1301-1307 ◽  
Author(s):  
Paul J. Tolentino ◽  
Anuradha Waghray ◽  
Kevin K. W. Wang ◽  
Ronald L. Hayes
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Tissue Type ◽  
Cerebral Artery Occlusion
Sign in / Sign up

Export Citation Format

Share Document