Article citationsMore>>

Hata, R., Maeda, K., Hermann, D., Mies, G. and Hossmann, K.A. (2000) Evolution of brain infarction after transient focal cerebral ischemia in mice. Journal of Cerebral Blood Flow & Metabolism, 20, 937-946. doi:10.1097/00004647-200006000-00006

has been cited by the following article:

• 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.