Effects of intracisternal tramadol on cerebral and spinal neuronal cells in rat

The aim was to investigate whether tramadol had toxic effect on cerebral neurons and/or spinal cord neurons when it was administered into the cerebrospinal fluid. Due to lipid peroxidation (LPO) and myeloperoxidation (MPO) levels are not specific predictors of neuronal damage, these biochemical markers of tissue damage were evaluated together with the histopathological findings of apoptosis.

Forty eight Wistar rats were anesthetized and the right femoral artery was cannulated. Mean arterial pressures, and heart rates, arterial carbon dioxide tension, arterial oxygen tension, blood pH were recorded. When the free cerebrospinal fluid flow was seen; 0.04 mL normal saline (Group Sham) or diluted tramadol in 0.04 mL volume (Group T1, T2, T0.5 and T0.1) was administered within 30 seconds from the posterior craniocervical junction of rats. For the Control Group, the free cerebrospinal fluid flow was seen but nothing was injected in it. After 7 days, following the sacrification of the rats, brain tissue, cervical and lumber segments of spinal cord were collected for the histopathological and biochemical examination.

There was not a statistically significant difference among all groups regarding the brain LPO levels (P=0.485). The LPO levels of the cervical segment of spinal cord and the lumbar segment of spinal cord were also similar (P=0.146, P=0.939, respectively). The mean MPO levels of the cervical and the lumbar segments of spinal cord were similar among all groups (P=0.693, P=0.377, respectively). There were not any statistically significant difference regarding the total number of red neurons of the brain tissue and the cervical and lumbar segments of spinal cord among all groups (P=0.264, P=0.202, P=0.780, respectively).

Tramadol had no neurotoxic effect on brain and on spinal cord tissue when administered by the intracisternal route in cerebrospinal fluid in rats.