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Background: Traumatic brain injury is still an important health problem worldwide. Traumatic brain injury not only causes direct mechanical damage to the brain but also induces biochemical changes that lead to secondary nerve cell loss. In this study, we investigated the neuroprotective effect of milrinone after traumatic brain injury (TBI) in a rat model., Methods: Forty male Wistar albino rats, were used. Rats were divided into 4 groups: 1) sham, 2) TBI, 3) TBI + Ringers, and 4) TBI + Milrinone. In group 1 (sham), only craniotomy was performed. In group 2 (TBI), TBI was performed after craniotomy. In group 3 (TBI + Ringer), TBI was performed after craniotomy and intraperitoneal Ringers solution was given immediately afterward. Group 4 (TBI + Milrinone), TBI was performed after craniotomy, and milrinone was given 1.0 mg/kg milrinone intraperitoneally directly (0.5 mg/kg milrinone intraperitoneally again 24 hours, 48 hours, and 72 hours after trauma). Tests were performed for neurological and neurobehavioral functions. Immunohistochemistry and histopathology studies were performed., Results: In group 4 compared with group 2 and group 3 groups, tests for neurological functions and neurobehavioral functions were significantly better. In the milrinone treatment used in group 4, plasma and brain tissue tumor necrosis factor, 8-OH 2-deoxyguanosine , and interleukin 6 levels were significantly decreased, and increased plasma and tissue IL-10 levels were detected. Histopathological spinal cord injury and apoptotic index increased in groups 2 and 3, while significantly decreasing in group 4., Conclusions: This study shows for the first time that the anti-inflammatory, antioxidant and antiapoptotic properties of milrinone may be neuroprotective after TBI., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Aim: Cerebral vasospasm after subarachnoid hemorrhage (SAH) is an important cause of morbidity and mortality. In this study, we examined the effects of L-carnitine on the cerebral vasospasm process., Material and Methods: Twenty male New Zealand white rabbits were randomly divided into 4 groups. Group 1 served as control; group 2 was not subjected to SAH and received intravenous L-carnitine 3 times; group 3 was subjected to SAH and group 4 was subjected to SAH and treated with 100 mg/kg intravenous L-carnitine at 0, 24, and 48 hours after SAH. All animals were euthanized by perfusion-fixation 72 hours after SAH induction. The brains were then removed and stored in fixative +4°C overnight. The subjects" basilar arteries were sectioned from four separate zones. Basilar artery cross-sectional areas and thicknesses of vessels were measured by using the SPOT for Windows Version 4.1 computer programme. Statistical comparisons were performed by using the Kruskal-Wallis and Mann-Whitney U tests., Results: Basilar artery wall thicknesses in group 4 were significantly lower than in group 3 (p=0.009). Basilar artery cross-sectional areas in group 4 were higher than in group 3 and the difference was statistically significant (p=0.008)., Conclusion: L-carnitine was shown to be potentially beneficial on the resolution of cerebral vasospasm following SAH.