Biochemical evidence of crossed cerebellar diaschisis in terms of nitric oxide indicators and lipid peroxidation products in rats during focal cerebral ischemia

Citation
M. Serteser et al., Biochemical evidence of crossed cerebellar diaschisis in terms of nitric oxide indicators and lipid peroxidation products in rats during focal cerebral ischemia, ACT NEUR SC, 103(1), 2001, pp. 43-48
Citations number
35
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
ACTA NEUROLOGICA SCANDINAVICA
ISSN journal
00016314 → ACNP
Volume
103
Issue
1
Year of publication
2001
Pages
43 - 48
Database
ISI
SICI code
0001-6314(200101)103:1<43:BEOCCD>2.0.ZU;2-D
Abstract
Objectives - Cerebral hypoperfusion in the contralateral cerebellar hemisph ere after stroke is interpreted as a functional and metabolic depression, p ossibly caused by a loss of excitatory afferent inputs on the corticopontoc erebellar pathway terminating in the cerebellar gray matter. This phenomeno n is defined as crossed cerebellar diaschisis and can be diagnosed clinical ly by positron emission tomography, single-photon emission computed tomogra phy, brain magnetic resonance imaging and electroencephalography in terms o f regional cerebral blood flow or metabolic rate of oxygen measurements. Ma terials and methods In the present study, nitric oxide indicators (nitrite and cyclic guanosine monophosphate) and lipid peroxidation products (malond ialdehyde and conjugated dienes) were measured in rat cerebral cortices and cerebella after permanent right middle cerebral artery occlusion in order to assess the crossed cerebellar diaschisis. Results - Nitrite values in ip silateral cortex were significantly higher than those in contralateral cort ex at 10 (P<0.001) and 60 (P<0.05) min of ischemia but no significant chang es were observed in both cerebellum compared to the 0 min values. In both c erebral cortex and cerebellum cGMP levels at 10 and 60 min were significant ly increased (P<0.001). This increase was marked in ipsilateral cortex and contralateral cerebellum when compared with opposite cortex and cerebellum (P<0.001). MDA values in ipsilateral cortex were significantly higher than those in contralateral cortex at 60 min of ischemia (P<0.05). Contralateral cerebellar MDA values were found significantly higher than those in ipsila teral cerebellum at 0 (P<0.001) and 60 (P<0.05) min of ischemia. In ipsilat eral cortex, conjugated diene values at 0, 10, 60 min of ischemia were high er than those in contralateral cortex. On the other hand 0, 10, 60 min conj ugated diene levels in contralateral cerebellum were significantly higher t han those in ipsilateral cerebellum (P<0.001). Conclusion - These findings support the interruption of the corticopontocerebellar tract as the mechani sm of the crossed cerebellar diaschisis.