scholarly journals Antibody to the α4 Integrin Decreases Infarct Size in Transient Focal Cerebral Ischemia in Rats

Stroke ◽  
2001 ◽  
Vol 32 (1) ◽  
pp. 206-211 ◽  
Author(s):  
Kyra Becker ◽  
Darin Kindrick ◽  
Jane Relton ◽  
John Harlan ◽  
Robert Winn
Keyword(s):  
Cerebral Ischemia ◽  
Infarct Size ◽  
Focal Cerebral Ischemia ◽  
Transient Focal Cerebral Ischemia

scholarly journals Inducible Nitric Oxide Synthase Does Not Mediate Brain Damage after Transient Focal Cerebral Ischemia in Mice

2007 ◽  
Vol 28 (3) ◽  
pp. 526-539 ◽  
Author(s):  
Harald Prüss ◽  
Konstantin Prass ◽  
Leyli Ghaeni ◽  
Milan Milosevic ◽  
Claudia Muselmann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Infarct Size ◽  
Focal Cerebral Ischemia ◽  
Inos Mrna ◽  
Wild Type ◽  
Transient Focal Cerebral Ischemia ◽  
Oxide Synthase ◽  
Deficient Mice ◽  
Inducible Nitric Oxide

Nitric oxide produced by the inducible nitric oxide synthase (iNOS) is believed to participate in the pathogenic events after cerebral ischemia. In this study, we examined the expression of iNOS in the brain after transient focal cerebral ischemia in mice. We detected differential expression of exons 2 and 3 of iNOS mRNA (16-fold upregulation at 24 to 72 h after middle cerebral artery occlusion, MCAO) compared with exons 6 to 8, 12 to 14, 21 to 22, and 26 to 27 (2- to 5-fold upregulation after 72 and 96 h), which would be compatible with alternative splicing. Expression levels of iNOS mRNA were too low for detection by the Northern blot analysis. Using specific antibodies, we did not detect any iNOS immunoreactivity in the mouse brain 1 to 5 days after MCAO, although we detected iNOS immunoreactivity in the lungs of mice with stroke-associated pneumonia, and in mouse and rat dura mater after lipopolysaccharide administration. In chimeric iNOS-deficient mice transplanted with wild-type bone marrow (BM) cells expressing the green fluorescent protein (GFP) or in wild-type mice transplanted with GFP+ iNOS-deficient BM cells, no expression of iNOS was detected in GFP+ leukocytes invading the ischemic brain or in resident brain cells. Moreover, both experimental groups did not show any differences in infarct size. Analysis of three different strains of iNOS-deficient mice and wild-type controls confirmed that infarct size was independent of iNOS deletion, but strongly confounded by the genetic background of mouse strains. In conclusion, our data suggest that iNOS is not a universal mediator of brain damage after cerebral ischemia.

Hyperbaric oxygen decreases infarct size and behavioral deficit after transient focal cerebral ischemia in rats

2000 ◽  
Vol 853 (1) ◽  
pp. 68-73 ◽  
Author(s):  
Roland Veltkamp ◽  
David S. Warner ◽  
Ferenc Domoki ◽  
Ann D. Brinkhous ◽  
James F. Toole ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Infarct Size ◽  
Hyperbaric Oxygen ◽  
Focal Cerebral Ischemia ◽  
Behavioral Deficit ◽  
Transient Focal Cerebral Ischemia

scholarly journals Chronic nicotine exposure exacerbates transient focal cerebral ischemia-induced brain injury

2016 ◽  
Vol 120 (3) ◽  
pp. 328-333 ◽  
Author(s):  
Chun Li ◽  
Hong Sun ◽  
Denise M. Arrick ◽  
William G. Mayhan
Keyword(s):  
Cerebral Cortex ◽  
Brain Injury ◽  
Cerebral Ischemia ◽  
Infarct Size ◽  
Focal Cerebral Ischemia ◽  
Neurological Deficits ◽  
Control Group ◽  
Nicotine Exposure ◽  
Chronic Nicotine ◽  
Transient Focal Cerebral Ischemia

Tobacco smoking is a risk factor contributing to the development and progression of ischemic stroke. Among many chemicals in tobacco, nicotine may be a key contributor. We hypothesized that nicotine alters the balance between oxidant and antioxidant networks leading to an increase in brain injury following transient focal cerebral ischemia. Male Sprague-Dawley were treated with nicotine (2 or 4 mg·kg−1·day−1) for 4 wk via an implanted subcutaneous osmotic minipump and subjected to a 2-h middle cerebral artery occlusion (MCAO). Infarct size and neurological deficits were evaluated at 24 h of reperfusion. Superoxide levels were determined by lucigenin-enhanced chemiluminescence. Expression of oxidant and antioxidant proteins was measured using Western blot analysis. We found that chronic nicotine exposure significantly increased infarct size and worsened neurological deficits. In addition, nicotine significantly elevated superoxide levels of cerebral cortex under basal conditions. Transient focal cerebral ischemia produced an increase in superoxide levels of cerebral cortex in control group, but no further increase was found in the nicotine group. Furthermore, chronic nicotine exposure did not alter protein expression of NADPH oxidase but significantly decreased MnSOD and uncoupling protein-2 (UCP-2) in the cerebral cortex and cerebral arteries. Our findings suggest that nicotine-induced exacerbation in brain damage following transient focal cerebral ischemia may be related to a preexisting oxidative stress via decreasing of MnSOD and UCP-2.

Reduction of infarct size by the NO donors sodium nitroprusside and spermine/NO after transient focal cerebral ischemia in rats

2000 ◽  
Vol 865 (2) ◽  
pp. 149-156 ◽  
Author(s):  
Juan B Salom ◽  
Marta Ortı́ ◽  
José M Centeno ◽  
Germán Torregrosa ◽  
Enrique Alborch
Keyword(s):  
Cerebral Ischemia ◽  
Infarct Size ◽  
Sodium Nitroprusside ◽  
Focal Cerebral Ischemia ◽  
No Donors ◽  
Transient Focal Cerebral Ischemia

Pre-ischemic depletion of brain norepinephrine decreases infarct size in normothermic rats exposed to transient focal cerebral ischemia

1999 ◽  
Vol 275 (3) ◽  
pp. 167-170 ◽  
Author(s):  
Bengt Nellgård ◽  
G Burkhard Mackensen ◽  
Shiva Sarraf-Yazdi ◽  
Yoshihide Miura ◽  
Robert Pearlstein ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Infarct Size ◽  
Focal Cerebral Ischemia ◽  
Brain Norepinephrine ◽  
Transient Focal Cerebral Ischemia

scholarly journals mGluR1 antagonist decreases tyrosine phosphorylation of NMDA receptor and attenuates infarct size after transient focal cerebral ischemia

2008 ◽  
Vol 105 (5) ◽  
pp. 1625-1634 ◽  
Author(s):  
Kazutoshi Murotomi ◽  
Norio Takagi ◽  
Gen Takayanagi ◽  
Megumi Ono ◽  
Satoshi Takeo ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Nmda Receptor ◽  
Infarct Size ◽  
Tyrosine Phosphorylation ◽  
Focal Cerebral Ischemia ◽  
Transient Focal Cerebral Ischemia
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