title: The effects of alpha lipoic acid on cerebral vasospasm following experimental subarachnoid hemorrhage in the rabbit.
abstract: OBJECTIVE
  The aim of this study is to determine the effects of a strong dithiol     antioxidant, alpha lipoic acid (ALA) on cerebral vasospasm following     subarachnoid hemorrhage in a rabbit model.
  
  
  METHODS
  Twenty-one New     Zealand white rabbits were assigned to one of three groups: group 1 (control),     group 2 (SAH only), group 3 (SAH+ALA). ALA was administered (100 mg/kg/day,     single dose, intraperitoneally). The rabbits were sacrificed 72 hours after SAH.     The basilar artery lumen areas, arterial wall thickness and endothelial     apoptosis in a cross section of basilar artery were measured in all groups. The     tissue MDA, SOD, GSH-Px levels were also determined.
  
  
  RESULTS
  The elevated     tissue MDA levels after SAH were significantly reduced by ALA treatment. The     reduced tissue SOD and GSH-Px levels after SAH were also elevated by ALA     treatment. In the treatment group the average wall thickness and the mean     percentages of apoptotic cells (apoptotic index) were reduced and the average     cross-sectional areas of the basilar artery were increased statistically     significantly.
  
  
  CONCLUSIONS
  ALA treatment attenuates the severity of cerebral     vasospasm by its strong antioxidant, antivasospastic and antiapoptotic     properties. ALA may potentially serve as agents in the prevention of cerebral     vasospasm after SAH.
authors.affiliation: M.H. Afsin State Hospital, Department of Neurosurgery, Afsin/ Kahramanmaras, Turkey. mfatiherdi@hotmail.com
authors.forename: Mehmet Fatih
authors.initials: MF
authors.lastname: Erdi
authors.forename: Onder
authors.initials: O
authors.lastname: Guney
authors.forename: Aysel
authors.initials: A
authors.lastname: Kiyici
authors.forename: Hasan
authors.initials: H
authors.lastname: Esen
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D001488:Basilar Artery / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000187:drug effects* / Q000378:metabolism; D005609:Free Radicals / Q000037:antagonists & inhibitors / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000037:antagonists & inhibitors / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000037:antagonists & inhibitors / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D011817:Rabbits; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000037:antagonists & inhibitors / Q000378:metabolism; D008063:Thioctic Acid / Q000494:pharmacology* / Q000627:therapeutic use; D016896:Treatment Outcome; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D020301:Vasospasm, Intracranial / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology*; D000094765:Glutathione Peroxidase GPX1
chemical_list: D000975:Antioxidants; D005609:Free Radicals; D008315:Malondialdehyde; D008063:Thioctic Acid; D006861:Hydrogen Peroxide; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D000094765:Glutathione Peroxidase GPX1