RESUMO
Objective To investigate the neuroprotective effect of vagus nerve stimulation ( VNS) on a model rat of focal cerebral ischemia. Methods A total of 42 adult male Sprague-Dawle ( SD) rats were randomly divided into a sham operation group (n=10),a model group (n=16),and a VNS-treated group ( n = 16 ) . Each group was randomly redivided into 2 subgroups:left VNS subgroup and right VNS subgroup. A model of focal cerebral ischemia (2 h) in rats was induced by the intraluminal suture method. At 30 minutes after modeling, the VNS-treated group received cervical VNS, the stimulation intensity was 0. 5 mA,the interval was 0. 5 ms,and the frequency was 20 Hz. Stimulation was once every 5 min within 1 h and each lasted for 30 s. The model group did not give any stimulation. Neither blood vessels were embolized nor were the nerves stimulated in the sham operation group. The changes of somatosensory evoked potentials ( SEP) on the lesion sides during operation were monitored. At 24 h after modeling,the neurobehavioral scores were performed. The rats were sacrificed,and their brain infarct volume was measured. Results (1) During the stimulation of left VNS in rats,the neurobehavioral scores of the sham operation group,model group and VNS-treated group were 0. 4 ± 0. 2,9. 5 ± 0. 4,6. 4 ± 0. 3,respectively;during the stimulation of right VNS in rats,the neurobehavioral scores of the 3 groups were 0. 6 ± 0. 2,9. 3 ± 0. 4,and 6. 9 ± 0. 4,respectively. There were significant differences between the scores of the model group and those of the other 2 groups (P0. 05). Conclusion No matter whether to stimulate the left or right vagus nerves, they both have neuroprotective effects on ischemic brain injury, and there was no significant difference on the action effects.
RESUMO
Objectives To investigate the neuroprotective mechanism of vagus nerve stimulation ( VNS) by stimulating the vagus nerve in ischemic cerebral tissue in a rat model of transient focal cerebral ischemia. Methods Twenty-six adult male Sprague-Dawley ( SD ) rats were randomly divided into sham operation group (n=6),model group (n=10),and VNS-treated group (n=10) . The model of rat transient focal cerebral ischemia was induced by the intraluminal suture method. At 30 min after modeling,the right side neck VNS in the VNS-treated group was stimulated ( stimulus intensity 0. 5 mA, interval 0. 5 ms, frequency 20 Hz),once every 5 min within 1 h,and once for 30 s. The model group repeated the steps of the VNS-treated group,but did not stimulate. The sham operation group repeated the experimental steps,but it neither embolized the vessels nor stimulated nerves. The changes of cerebral blood flow were monitored with a laser Doppler flowmeter. The rats were sacrificed after 24 h. The expressions of interleukin 6(IL-6) and caspase-3 in brain tissue were determined by immunohistochemistry staining. The neuronal apoptosis was observed by the in situ end-labelling technique. Results ( 1 ) Compared with the sham operation group, the number of positive cells of IL-6,caspase-3,and the numbers of neuronal apoptosis in the model group were significantly increased (20. 7 ± 5. 0 cells/HP vs. 2. 3 ± 1. 0 cells/HP,44. 5 ± 9. 5 cells/HP vs. 0,30. 9 ± 9. 0 cells/HP vs.0).Thereweresignificantdifferences(P0. 05). Conclusion The neuroprotective mechanism of VNS for cerebral ischemia may be associated with the inhibition of neuronal apoptosis and decreasing inflammatory response. It may not be associated with the changes of cortical cerebral blood flow.