The aim of this study was to investigate the effect of vagus nerve stimulation (VNS) on infarct volume and neurological recovery up to 3 weeks following transient focal cerebral ischemia. Transient ischemia was produced by filament occlusion of the proximal middle cerebral artery (MCA) in rats. The right vagus nerve was stimulated starting 30 min after MCA occlusion and consisted of 30-sec pulse trains (20 Hz) delivered to the animal's right vagus nerve every 5 min for a total period of 60 min (n = 10). All the procedures were duplicated, but no stimulus was delivered, in a control group (n = 10). Neurological evaluations were performed in all animals at 24 hr, 48 hr, 1 week, 2 weeks, and 3 weeks after MCA occlusion; animals were euthanized; and neuronal damage was evaluated in hematoxylin-eosin-stained sections. The ischemic lesion volume was smaller in the VNS-treated animals in comparison with the nonstimulated group (P < 0.02). Although the functional score in both treated and untreated groups improved over the 3-week observation period (P < 0.001), there was still a statistically significant improvement reszulting from VNS treatment compared with control animals (P < 0.05). Cerebral blood flow changes in the MCA territory during ischemia did not differ between the VNS-treated animals (31.9% ± 10.4% of baseline) and control animals (29.9% ± 9.1%; P = 0.6). Stimulation of the vagus nerve for only a brief period early in ischemia provides neuroprotection in transient ischemia, with neuroprotection persisting for at least 3 weeks.
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Hiraki et al. (2011) studied this question.
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