1232 Essential role of endogenous tissue plasminogen activator in hemorrhage transformation after ischemia/reperfusion in transient focal cerebral ischemia rats

2005 ◽  
Vol 238 ◽  
pp. S414
Keyword(s):  
Cerebral Ischemia ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Essential Role ◽  
Focal Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Transient Focal Cerebral Ischemia ◽  
Tissue Plasminogen

Aggravation of focal cerebral ischemia by tissue-plasminogen activator is reversed by rosuvastatin - role of endothelial NO synthase

2004 ◽  
Vol 31 (S 1) ◽  
Author(s):  
E Kilic ◽  
Ü Kilic ◽  
C Matter ◽  
T Lüscher ◽  
C Bassetti ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Focal Cerebral Ischemia ◽  
No Synthase ◽  
Endothelial No Synthase ◽  
Tissue Plasminogen

Effects of tissue plasminogen activator on cerebral microvessels of rats during focal cerebral ischemia and reperfusion

2007 ◽  
Vol 29 (3) ◽  
pp. 274-282 ◽  
Author(s):  
Dar-Yu Yang ◽  
Hung-Chuan Pan ◽  
Chun-Jung Chen ◽  
Fu-Chou Cheng ◽  
Yeou-Chih Wang
Keyword(s):  
Cerebral Ischemia ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Focal Cerebral Ischemia ◽  
Ischemia And Reperfusion ◽  
Cerebral Microvessels ◽  
Cerebral Ischemia And Reperfusion ◽  
Tissue Plasminogen

Long-lasting neuronal loss following experimental focal cerebral ischemia is not affected by combined administration of tissue plasminogen activator and hyperbaric oxygen

2011 ◽  
Vol 1417 ◽  
pp. 115-126 ◽  
Author(s):  
Carsten Hobohm ◽  
Félix Laignel ◽  
Johannes Kacza ◽  
Lea Küppers-Tiedt ◽  
Marita Heindl ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Hyperbaric Oxygen ◽  
Focal Cerebral Ischemia ◽  
Neuronal Loss ◽  
Tissue Plasminogen ◽  
Combined Administration

Abstract WMP82: Inhibition of Thioredoxin Interacting Protein Attenuates Tissue Plasminogen Activator Induced Brain Damage Under Acute Hyperglycemia in Murine Stroke Model

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Saifudeen Ismael ◽  
Lexiao Li ◽  
Arum Yoo ◽  
Tauheed Ishrat
Keyword(s):  
Cerebral Ischemia ◽  
Infarct Size ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Focal Cerebral Ischemia ◽  
Interacting Protein ◽  
Acute Hyperglycemia ◽  
Thioredoxin Interacting Protein ◽  
Blood Brain ◽  
Tissue Plasminogen

Background and Hypothesis: Acute hyperglycemia (AHG) worsens stroke outcome and increases the risk of intracerebral hemorrhage after tissue plasminogen activator (tPA) treatment, independent of preexisting diabetes. We have previously reported that genetic deletion of thioredoxin interacting protein exerts neuroprotection after experimental stroke. Here we tested the hypothesis that pharmacological inhibition of TXNIP, with verapamil protects against tPA-induced brain damage under AHG in a mouse model of focal cerebral ischemia. Methods: Transient focal cerebral ischemia was induced by a 60 min middle cerebral artery occlusion (MCAO) followed by 23 h reperfusion in mice. AHG was induced by administration of 20% glucose (ip), 15 minutes before MCAO. Verapamil (0.015 mg/kg, iv) and tPA (iv), or saline was administered at 1 h post-occlusion. After 24 h of I/R, mice were tested for neurobehavioral outcome and were evaluated for infarct size and expression inflammatory mediators, and blood brain barrier markers. Results: AHG aggravated brain edema, blood brain disruption and neuroinflammation. Treatment with verapamil significantly reduced in the infarct size (41%, p<0.05), hemorrhage (36%) and edema (36%, p<0.05) compared to saline treated controls. Furthermore, verapamil significantly inhibited the TXNIP mediated activation of NLRP3-inflammsome and ameliorated blood brain barrier leakage (Table 1). Conclusion: Taken together, these data indicate that inhibition of TXNIP with verapamil may have therapeutic implications on ischemic stroke in the acute hyperglycemic condition.

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