Time Course of Postischemic Stroke Symptoms and Delayed Infarction After Transient Cerebral Ischemia in Gerbils: Effect of Chemical Preconditioning Using 3-Nitropropionic Acid

2001 ◽  
pp. 141-145
Author(s):  
T. Kuroiwa ◽  
I. Yamada ◽  
Y. Hakamata ◽  
K. Ohno ◽  
S. Endo ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Time Course ◽  
Transient Cerebral Ischemia ◽  
Nitropropionic Acid ◽  
3 Nitropropionic Acid

scholarly journals Tolerance-Inducing Dose of 3-Nitropropionic Acid Modulates bcl-2 and bax Balance in the Rat Brain: A Potential Mechanism of Chemical Preconditioning

2000 ◽  
Vol 20 (10) ◽  
pp. 1425-1436 ◽  
Author(s):  
Ansgar M. Brambrink ◽  
Armin Schneider ◽  
Holger Noga ◽  
Andreas Astheimer ◽  
Bernhard Götz ◽  
...  
Keyword(s):  
Single Dose ◽  
Cerebral Ischemia ◽  
Protein Expression ◽  
Ischemia Reperfusion ◽  
Global Cerebral Ischemia ◽  
Mrna Levels ◽  
Nitropropionic Acid ◽  
Bax Protein ◽  
Cerebral Ischemia Reperfusion ◽  
3 Nitropropionic Acid

Many studies have reported ischemia protection using various preconditioning techniques, including single dose 3-nitropropionic acid (3-NPA), a mitochondrial toxin. However, the cellular signal transduction cascades resulting in ischemic tolerance and the mechanisms involved in neuronal survival in the tolerant state still remain unclear. The current study investigated the mRNA and protein expression of the antiapoptotic bcl-2 and the proapoptotic bax, two antagonistic members of the bcl-2 gene family, in response to a single dose of 3-NPA, to global cerebral ischemia–reperfusion, and to the combination of both 3-NPA-pretreatment and subsequent global cerebral ischemia–reperfusion. Brain homogenates of adult Wistar rats (n = 25) were analyzed for bcl-2 and bax mRNA expression using a new highly sensitive and quantitative polymerase chain reaction (PCR) technique that allows real-time fluorescence measurements of the PCR product (LightCycler; Roche Diagnostics, Mannheim, Germany). Animals for mRNA analysis received 3-NPA (20 mg/kg, intraperitoneal; “chemical preconditioning”) or vehicle (normal saline), and were either observed for 24 plus 3 hours or were subjected to 15 minutes of global cerebral ischemia 24 hours after the pretreatment and observed for 3 hours of reperfusion. Immunohistochemistry was applied to serial brain sections of additional rats (n = 68) to determine amount and localization of the respective Bcl-2 and Bax protein expression in various brain areas. One set of animals was injected with 3-NPA and observed for 3, 12, 24, and 96 hours; a second set was exposed to 15 minutes global cerebral ischemia, 3, 12, and 24 hours reperfusion; and a third set was pretreated with 3-NPA or saline 24 hours before the ischemic brain insult and observed for 96 hours of reperfusion. The authors found single dose 3-NPA treatment to be associated with an elevated bcl-2:bax ratio (increased bcl-2 expression, decreased bax expression), both on the transcriptional (mRNA) and the translational (protein) level. The differential influence of 3-NPA was maintained during early recovery from global cerebral ischemia (3 hours), when 3-NPA pretreated animals showed higher bcl-2 and lower bax mRNA levels compared with rats with saline treatment. Respective changes in protein expression were localized predominately in neurons vulnerable to ischemic damage. Compared with baseline, Bcl-2 protein was significantly higher in surviving neurons at 96 hours after the insult, whereas Bax protein remained unchanged. However, at this late time of postischemic recovery (96 hours), the protein expression pattern of surviving neurons was not different between animals with and without 3-NPA pretreatment. To the authors' knowledge, the current study is the first report on the differential expression of pro-and antiapoptotic genes after a single, nonlethal dose of 3-NPA. The current results suggest alterations in the balance between pro-and antiapoptotic proteins as a potential explanation for the reported protection provided by chemical preconditioning using 3-NPA in rats.

scholarly journals Time course of oxidative damage in different brain regions following transient cerebral ischemia in gerbils

2001 ◽  
Vol 41 (3) ◽  
pp. 233-241 ◽  
Author(s):  
Eduardo Candelario-Jalil ◽  
Noël H. Mhadu ◽  
Said M. Al-Dalain ◽  
Gregorio Martı́nez ◽  
Olga Sonia León
Keyword(s):  
Cerebral Ischemia ◽  
Oxidative Damage ◽  
Time Course ◽  
Brain Regions ◽  
Transient Cerebral Ischemia

Time-course Changes in Immunoreactivities of Glucokinase and Glucokinase Regulatory Protein in the Gerbil Hippocampus Following Transient Cerebral Ischemia

2013 ◽  
Vol 38 (12) ◽  
pp. 2640-2649 ◽  
Author(s):  
Joon Ha Park ◽  
Choong Hyun Lee ◽  
In Hye Kim ◽  
Ji Hyeon Ahn ◽  
Jeong-Hwi Cho ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Time Course ◽  
Regulatory Protein ◽  
Transient Cerebral Ischemia ◽  
Glucokinase Regulatory Protein ◽  
Course Changes

scholarly journals Evaluation of Lactate Production and Clearance Kinetics by 1H NMR in a Model of Brief Repetitive Cerebral Ischemia

1994 ◽  
Vol 14 (4) ◽  
pp. 591-596 ◽  
Author(s):  
Hoby P. Hetherington ◽  
Min-Jie Tan ◽  
Kang-Li Luo ◽  
Gerald M. Pohost ◽  
James H. Halsey ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
High Performance ◽  
Time Course ◽  
Lactate Production ◽  
Transient Cerebral Ischemia ◽  
Specific Level ◽  
Lactate Accumulation ◽  
Gravitational Stress ◽  
The Individual

Pilots of high-performance aircraft are subject to repeated transient cerebral ischemia during high-gravitational stress maneuvers. Previously we have demonstrated that repeated episodes of transient cerebral ischemia and reflow are cumulative and lactate accumulations appear to be exponential. To evaluate the metabolic events determining the kinetics of lactate accumulation, and therefore the rates of substrate utilization, we have used in vivo 1H nuclear magnetic resonance with a 5-s time resolution to measure lactate production and clearance. The individual rates for each animal were then used to predict the accumulation of lactate in the same animal during 30 episodes of ischemia and reflow. Lactate accumulation was modeled as the balance between a zero-order production process during the ischemic period and a first-order clearance process. The predicted lactate accumulation showed excellent agreement with the observed time course, validating the predictive power of the simple model used. The highly reproducible nature of this model and its accuracy in predicting lactate accumulation should enable more accurate studies of the deleterious effects of lactate accumulation in cerebral ischemia by providing a highly reproducible means for generating a specific level of lactate accumulation.

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