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