Authors: HongGang Zhao XiaoCai Sun XiaoHui Xian WenBin Li Min Zhang QingJun Li
Publish Date: 2007/06/06
Volume: 32, Issue: 11, Pages: 1919-1926
Abstract
Brief limb ischemia was reported to protect neurons against injury induced by subsequent cerebral ischemiareperfusion and this phenomenon is known as limb ischemic preconditioning LIP To explore the role of nitric oxide NO in neuroprotection of LIP in rats we observed changes in the content of nitric oxide NO and activity of NO synthase NOS in the serum and CA1 hippocampus of rats after transient limb ischemic preconditioning LIP and the influence of NGnitrolarginine methylester lNAME a NOS inhibitor on the neuroprotection of LIP against cerebral ischemiareperfusion injury Results showed that NO content and NOS activity in serum increased significantly after LIP compared with the sham group The increase showed a double peak pattern in which the first one appeared at time 0 immediate time point and the second one appeared at 48 h after the LIP P 001 The NO content and NOS activity in the CA1 hippocampus in LIP group showed similar change pattern with the changes in the serum except for the first peak of upregulation of NO content and NOS activity appeared at 6 h after LIP Pretreatment with lNAME before LIP blocked the neuroprotection of LIP against subsequent cerebral ischemic insult The blocking effect of lNAME was abolished with pretreatment of lArg These findings indicated that NO may be associated with the tolerance of pyramidal cells in the CA1 hippocampus to ischemia induced by LIP in rats
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