Author(s): Jelenković Ankica, Jovanović Marina, Ninković Milica, Maksimović M, Bošković B
Keywords:brain, lipid peroxidation, nitric oxide, oxidative stress, pentobarbital, surgery
It is expected that clinical recovery after surgically induced brain trauma is followed by molecular and biochemical restitution. Seven days after surgery, we investigated whether the plastic cannula implanted in the left brain ventricle of adult Wistar rats (n=6-7), performed in pentobarbital anesthesia, could influence oxidative stress elements (superoxide anion and lipid peroxidation), as well as the antioxidative system (superoxide dismuthase-SOD). Also, we investigated whether nitric oxide (NO) is involved in these processes. Biochemical analyses was performed in the forebrain cortex, striatum and hippocampus. Clinical recovery was complete seven days after surgery. Thereafter, thirty minutes before decapitation, through the cannula, one group of rats received saline intracerebroventricularly (control group), and the treated group receaved N-nitro-L-arginine methyl ester (LNAME). The third group was left unoperated and untreated. Before and after the treatments, rectal body temperature was measured. Compared to the untreated group the index of lipid peroxidation was increased in all three brain structures in the group that received saline (p<0.05 to 0.01). Application of L-NAME deteriorated it in the striatum and hippocampus (p<0.01 compared to the both other groups), but the value in the forebrain cortex was similar to the untreated group. Supeoxide anion level was decreased in the L-NAME treated group only in the striatum (p<0.01 compared to control and untreated groups), but SOD was increased in the hipppocampus, compared to the saline treated group (p<0.05). Seven days after brain surgery in pentobarbital anesthesia, recovery of biochemical disturbances was not parallel to clinical recovery. Long lasting biochemical changes are rather the consequence of brain injury than to pentobarbital anesthesia. In this experimental model, NO had protective effects, acting against lipid peroxidation in the striatum and hippocampus, but not in the forebrain cortex i. e. NO involvement in the free radical processes strongly depends on the observed brain region.
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