Effect of Mannitol Infusion on Optic Nerve Injury After Acute Traumatic Subarachnoid Hemorrhage and Brain Injury

J Craniofac Surg. 2018 Oct;29(7):1772-1775. doi: 10.1097/SCS.0000000000004827.

Abstract

The primary aim of this paper is to investigate the neuroprotective and antiinflammatory effects of mannitol on optic nerve injury after acute traumatic subarachnoid hemorrhage and brain injury in rat models. Traumatic brain injury (TBI) and traumatic subarachnoid hemorrhage (tSAH) were produced by a custom-made weight-drop impact acceleration device. Thirty male Wistar rats were divided into 3 groups. Group I (n = 10) was the sham group, group II (n = 10) received TBI, and group III (n = 10) received TBI + mannitol (1 mg/kg intravenously). Optic nerve tissue glutathione peroxidase (GPx) and interleukin 1 beta (IL-1β) levels were measured 4 hours after the trauma. The authors used Kruskal-Wallis variance analysis and Mann-Whitney U tests for statistical analysis. Optic nerve tissue GPx levels were significantly higher in group III than in groups I and II (P < 0.05). Optic nerve tissue IL-1β levels were significantly lower in group III than in group II (P < 0.05) and higher than in group I (P < 0.05).Mannitol increased the antioxidant GPx levels and decreased the IL-1β levels, which can protect the optic nerve from secondary injury after severe acute trauma. Mannitol plays an important role in the treatment of acute severe indirect optic nerve injury after TBI and tSAH.

MeSH terms

  • Animals
  • Glutathione Peroxidase / metabolism*
  • Interleukin-1beta / metabolism*
  • Male
  • Mannitol / therapeutic use*
  • Neuroprotective Agents / therapeutic use*
  • Optic Nerve Injuries / drug therapy*
  • Optic Nerve Injuries / etiology
  • Optic Nerve Injuries / metabolism*
  • Rats
  • Rats, Wistar
  • Subarachnoid Hemorrhage, Traumatic / complications

Substances

  • IL1B protein, rat
  • Interleukin-1beta
  • Neuroprotective Agents
  • Mannitol
  • Glutathione Peroxidase