Objective: To study the protective effect of electrical stimulating cerebellar fastigial nucleus on ischemia-reperfusion-injury of rat retina.
Methods: Rats were divided randomly into group of ischemia-reperfusion, group of electrical-stimulation-treated and group of sham-operated. The duration ischemia was 1 hour except sham-operated. In treated group, harvests of retinas followed electrical stimulation of cerebellar fastigial nucleus for 60 min after reperfusion for 6 hours; in reperfusion group, retinas were harvested only after 6 hours reperfusion. Retinal ischemia was produced in rats by ligating vessels and the optic nerve for 1 hour. Expression of inducible nitric oxide synthase (iNOS) in retina was measured by NADPH-NDP histochemistry; Apoptosis was measured by Tdt-dUTP terminal nick-end labeling (TUNEL) method. Morphology change was observed with the help of HPIAS-1000 auto-medical-imagined computer analyzer.
Results: (1) The thickness of inner retinal (including outer plexiform layer, inner nuclear layer, ganglion cell layer, optic nerve fiber and inner limiting membrane) and the inner plexiform layer were increased significantly in ischemia-reperfusion group than those in treated group. (2) The morphological changes of the scattered and condensed nucleus were observed more slightly under light microscopy in treated group than those in ischemia-reperfusion group. (3) Expression of inducible nitric oxide synthase (iNOS) in retinal ganglion cell in treated group is more significant than in ischemia-reperfusion group. (4) The amount of apoptosis cells in retina in treated group is significantly less than thatin ischemia-reperfusion group.
Conclusions: (1) The results indicated that ischemia-reperfusion injury can induce retinal apoptosis. Retinal apoptosis can be inhibited by electrical stimulation cerebellar fastigial nucleus. (2) iNOS maybe involved in the mechanism of apoptosis. (3) Cerebellar fastigial nucleus electrical stimulation can protect ischemia-reperfused retina.