Neuroprotective Effects of Milrinone on Experimental Acute Spinal Cord Injury: Rat Model

Abstract Objective Spinal cord injury (SCI) disrupts nerve axons with devastating neurological consequences, but there is no effective clinical treatment. The secondary damage mechanism is a mainstay process, and it starts within a few minutes after trauma. We aim to investigate the neuroprotective effects of milrinone on the spinal cord injury model. Materials and Methods 36 Wistar albino rats, each weighing 300-400g, were randomly split into four groups that received different treatments: in Group 1 (sham) (n: 9) control, only a laminectomy was performed; in Group 2 (SCI) (n: 9), SCI was imitated after laminectomy; in Group 3 (SCI+ Saline) (n: 9), physiological saline solution was injected intraperitoneally immediately after the SCI and in Group 4 (SCI+Milrinone), milrinone was administered intraperitoneally on lateral decubitus position immediately after the SCI. Spinal cord contusion was established by the weight-drop technique after laminectomy. Neurological examination scores were recorded, and rats were sacrificed 72 hours later. Serum and spinal cord tissue glutathione peroxidase (GPx), total antioxidant status (TAS), total oxidant status (TOS), 8-hydroxiguanosine (8-OHdG), interleukin-6 (IL-6) and interleukin-10 (IL- 10) levels, histopathological spinal cord damage score and apoptotic index were examined and compared between groups. Results Neurological examination scores were significantly better in milrinone treated group compared to groups 2 and 3. SCI significantly increased serum and spinal cord tissue GPx, TOS, 8- OHdG, and IL-6 levels which were successfully reduced with milrinone treatment. IL-10 and TAS levels decreased as a result of SCI increased with milrinone treatment. Increased histopathological spinal cord damage score and apoptotic index in groups 2 and 3, significantly decreased in group 4. Conclusions Milrinone could reduce apoptosis, increase anti-inflammatory and anti-oxidative mediators, thus playing a protective role in secondary nerve injury after SCI in rats