Tumor necrosis factor-$alpha; does not modulate ischemia/reperfusion injury in na�ve myocardium but is essential for the development of late preconditioning*1

Author(s):  
B DAWN
2001 ◽  
Vol 120 (5) ◽  
pp. A196-A197
Author(s):  
Peter C. Konturek ◽  
Tomasz Brzozowski ◽  
Aleksandra Duda ◽  
Slawomir Kwiecien ◽  
Holger Meixner ◽  
...  

1998 ◽  
Vol 18 (1) ◽  
pp. 52-58 ◽  
Author(s):  
Sean D. Lavine ◽  
Florence M. Hofman ◽  
Berislav V. Zlokovic

The role of tumor necrosis factor-alpha (TNF-α) in brain injury is controversial. We studied the effect of anti–TNF-α antibody in a rat model of reversible middle cerebral artery occlusion. During focal ischemia and early reperfusion, TNF-α was rapidly and transiently released into circulation. Pretreatment with intravenous anti–TNF-α antibody reduced cortical (71%, P < 0.015) and subcortical (58%, P < 0.007) injury, enhanced the cerebral blood flow during reperfusion, and improved the neurologic outcome. This further supports the contention that TNF-α is a deleterious cytokine in stroke, whereas circulating antibody against TNF-α may protect brain from reperfusion injury.


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