Article citationsMore>>
Dave, K.R., Saul, I., Busto, R., Ginsberg, M.D., Sick, T.J. and Perez-Pinzon, M.A. (2001) Ischemic preconditioning preserves mitochondrial function after global cerebral ischemia in rat hippocampus. Journal of Cerebral Blood Flow & Metabolism, 21, 1401-1410.
doi:10.1097/00004647-200112000-00004
has been cited by the following article:
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TITLE:
Down-regulation of Rho-kinases induce tolerance in Ischemic preconditioning model after transient cerebral ischemia/reperfusion in rats
AUTHORS:
Hiba A. Awooda
KEYWORDS:
Cerebral; Ischemic Preconditioning; ROCK; NO
JOURNAL NAME:
Health,
Vol.5 No.7E,
July
18,
2013
ABSTRACT: Background: Ischemic preconditioning (IPC) is a brief
episode of ischemia/reperfusion (I/R) that protects the brain from the damage
induced by subsequent prolonged ischemia. Aim: To study the neuroprotective mechanism of IPC. Methods: 30 adult
male Wistar rats (150-250 g) were divided into three groups 10 rats in each; the
first group was sham-operated and served as a control, I/R group of rats
subjected to 30 minutes of left common carotid artery occlusion (CCAO) followed
by 24-hour of reperfusion, IPC group were treated with three episodes of 5-minutes
of CCAO with 10 minutes of reperfusion in between, followed by 30 minutes of
CCAO and then allowed for reperfusion for 24 hours. Neurobehavioral
assessments were evaluated; Rhokinases (ROCK) and nitrite were measured in
affected cerebral hemisphere. Results: Rats’ neurological deficits were
significantly decreased in the I/R compared with the control group (P contrast,
the ROCK level was significantly higher in I/R group compared to control
group and its level significantly decreased in IPC rats when compared to I/R
group (P 0.695, P = 0.000). Conclusions: Downregulation of
ROCK level following preconditioning stimuli with the potential involvement
of Nitric oxide (NO) appear to be one of the neuroprotective mechanisms of IPC protection against a subsequent I/R
challenge evidence by improvement in the neurological deficits.