چنسو وانگ

Statins have been used in neuroprotection after cerebral ischemia. However, their mechanisms of action remain unknown. We have previously shown the protective effect of statins after cerebral ischemic injury. We have also shown that hyperthermia can exacerbate cerebral ischemic injury and that the efficacy of tissue plasminogen activator (tPA) is reduced in the presence of hyperthermia. In this study the effect of simvastatin alone or in combination with hyperthermia on brain ischemic injury was evaluated. This was an experimental study. Sample size comprised 13 groups of male rats. In four studies, the rectal and brain temperature of the rats were measured and neuroprotective effect of simvastatin alone or in combination with hyperthermia in thromboebolic stroke was evaluated. The collected data were analyzed by means of sigmastat 3.1 soft ware and statistical tests of ANOVA, Tukey and Krascal walis. The results of this study showed that brain temperature was approximately 0.50C lower than that of rectum. Results indicate that simvastatin alone reduced the infarct volume by 46% compared to the control group (p<0.01). Simvastatin improved neurological deficits and reduced brain edema significantly, (p<0.05). Administration of simvastatin significantly decreased perfusion deficits and BBB permeability. These studies suggest that simvastatin is protective in an embolic model of stroke and can decrease BBB permeability and perfusion deficits in brain injured rats.MCA: middle cerebral artery, BBB: blood- brain barrier, tPA: tissue plasminogen activator