scholarly journals Tissue processing and optimal visualization of cerebral infarcts following sub-acute focal ischemia in rats

2021 ◽  
Vol 118 ◽  
pp. 102034
Author(s):  
Vibeke Bay ◽  
Nina K. Iversen ◽  
Seyedeh Marziyeh Jabbari Shiadeh ◽  
R. Andrew Tasker ◽  
Gregers Wegener ◽  
...  
2010 ◽  
Vol 34 (8) ◽  
pp. S16-S16
Author(s):  
Fang‑fang Bi ◽  
Hadi M. Mujlli ◽  
Yue‑qiang Hu ◽  
Fa‑fa Tian ◽  
Zhi‑guo Wu ◽  
...  

2005 ◽  
Vol 32 (S 4) ◽  
Author(s):  
A Kunze ◽  
S Grass ◽  
O.W Witte ◽  
G Kempermann ◽  
C Redecker

2020 ◽  
Vol 14 (4) ◽  
pp. 329-334
Author(s):  
T. N. Fedorova ◽  
V. S. Gusakov ◽  
A. A. Devyatov ◽  
O. A. Muzichuk ◽  
A. V. Lopachev ◽  
...  
Keyword(s):  

Circulation ◽  
2000 ◽  
Vol 102 (Supplement 3) ◽  
pp. III-210-III-215 ◽  
Author(s):  
B. Pouzet ◽  
J.-T. Vilquin ◽  
A. A. Hagege ◽  
M. Scorsin ◽  
E. Messas ◽  
...  

1999 ◽  
Vol 19 (6) ◽  
pp. 652-660 ◽  
Author(s):  
Jaroslaw Aronowski ◽  
Ki-Hyun Cho ◽  
Roger Strong ◽  
James C. Grotta

To determine the occurrence and time-course of presumably irreversible subcellular damage after moderate focal ischemia, rats were subjected to 1, 3, 6, 9, or 24 hours of permanent unilateral middle cerebral and common carotid occlusion or 3 hours of reversible occlusion followed by 3, 6, or 21 hours of reperfusion. The topography and the extent of damage were analyzed with tetrazolium staining and immunoblot using an antibody capable of detecting breakdown of neurofilament. Neurofilament proteolysis began after 3 hours in the infarct core but was still incomplete in penumbral regions up to 9 hours. Similarly, tetrazolium-staining abnormalities were observed in the core of 50% of animals after 3 hours of ischemia. At 6 hours of permanent ischemia, infarct volume was maximal, and further prolongation of occlusion to 9 or 24 hours did not increase abnormal tetrazolium staining. In contrast to permanent ischemia and in agreement with the authors' previous demonstration of “reperfusion injury” in this model, prolongation of reperfusion from 3 hours to 6 and 21 hours after 3 hours of reversible occlusion gradually augmented infarct volume by 203% and 324%, respectively. Neurofilament proteolysis initiated approximately 3 hours after ischemia was quantitatively greatest in the core and extended during reperfusion to incorporate penumbra with a similar time course to that of tetrazolium abnormalities. These data demonstrate that, at least as measured by neurofilament breakdown and mitochondrial failure, extensive cellular damage is not present in penumbral regions for up to 9 hours, suggesting the potential for rescuing these regions by appropriate and timely neuroprotective strategies.


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