Ilknur Ay1, Jie Lu, Hakan Ay, A Gregory Sorensen. 1. MGH/MIT/HMS A.A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital-East, 149 13th Street, Charlestown, MA O2129, USA. iay@partners.org
Abstract
BACKGROUND AND PURPOSE: We sought to determine the effect of vagus nerve stimulation (VNS) on infarct size after transient focal cerebral ischemia in rats. METHODS: Ischemia was produced by transient filament occlusion of the right middle cerebral artery. Stimulating electrodes were implanted on the cervical part of the right vagus nerve. Electrical stimulation was initiated 30 min after the induction of ischemia, and delivered for 30s at every 30 min for 3h in experimental group 1 and at every 5 min for 1h in experimental group 2. All the procedures were duplicated but no stimulus was delivered in the control group. Functional deficit was evaluated and animals were killed to determine the infarct size 24h after ischemia. RESULTS: Ischemic lesion volume was smaller in VNS-treated animals as compared with control animals; the relative percentage of contralateral hemispheric volume that underwent infarction was 16.2+/-3.2% in the VNS and 33.0+/-5.0% in the control arms in experimental group 1 (p<0.05). The respective values for experimental group 2 were 19.8+/-0.5% and 37.9+/-2.6% (p<0.05). VNS-treated animals were significantly more likely to have better functional scores at 24h as compared with control animals. The functional score improved by 50% in experimental group 1 and 44% in experimental group 2 (p<0.05 for both groups). CONCLUSION: VNS appears to offer protection against acute ischemic brain injury.
BACKGROUND AND PURPOSE: We sought to determine the effect of vagus nerve stimulation (VNS) on infarct size after transient focal cerebral ischemia in rats. METHODS:Ischemia was produced by transient filament occlusion of the right middle cerebral artery. Stimulating electrodes were implanted on the cervical part of the right vagus nerve. Electrical stimulation was initiated 30 min after the induction of ischemia, and delivered for 30s at every 30 min for 3h in experimental group 1 and at every 5 min for 1h in experimental group 2. All the procedures were duplicated but no stimulus was delivered in the control group. Functional deficit was evaluated and animals were killed to determine the infarct size 24h after ischemia. RESULTS: Ischemic lesion volume was smaller in VNS-treated animals as compared with control animals; the relative percentage of contralateral hemispheric volume that underwent infarction was 16.2+/-3.2% in the VNS and 33.0+/-5.0% in the control arms in experimental group 1 (p<0.05). The respective values for experimental group 2 were 19.8+/-0.5% and 37.9+/-2.6% (p<0.05). VNS-treated animals were significantly more likely to have better functional scores at 24h as compared with control animals. The functional score improved by 50% in experimental group 1 and 44% in experimental group 2 (p<0.05 for both groups). CONCLUSION: VNS appears to offer protection against acute ischemic brain injury.