Kocaogullar, YUstun, MEAvci, EKarabacakoglu, AFossett, D2020-03-262020-03-2620040342-46421432-1238https://dx.doi.org/10.1007/s00134-003-1916-7https://hdl.handle.net/20.500.12395/19258Objective: To determine the role of hyperoxic and hyperbaric therapy following experimental subarachnoid hemorrhage (SAH). Design: Prospective, randomized, controlled animal study. Subjects: Thirty male Wistar rats. Interventions: Thirty rats were assessed for an initial neurologic status as double-blinded by two different neurosurgeons using a neurologic severity score (NSS) and then underwent an initial angiographic examination. Two days later, 0.3 ml of homologous blood was injected into the cisterna magna to produce a SAH-induced cerebral vasospasm. The NSS and angiographic examination were then repeated. The rats having no spasm or a spasm under 50% (n=8) and 50% or over 50% (n=22) were grouped separately, as groups 1 and 2, respectively. The rats having 50% or more spasm were further divided randomly into group 2A and 2B. The rats in groups 1 and 2A (n= 11) underwent a 60-min course of 100% oxygen at the atmospheric pressure 1 atmosphere absolute (ata), and group 2B (n= 11) received 100% oxygen at 3 ata for I h. Neurologic assessment was repeated on the next day and 7 days later. Measurements and main results: The animals having no spasm or less than 50% spasm had a better NSS and outcome when compared with the animals having 50% or more spasm. But the animals with 50% or more spasm which underwent hyperbaric therapy were shown to have a better outcome compared to the animals having hyperoxic therapy. Conclusion: Exposure to hyperbaric oxygen therapy seemed to accelerate the recovery of neurologic deficits secondary to experimental SAH.en10.1007/s00134-003-1916-7info:eu-repo/semantics/openAccesssubarachnoid hemorrhagehyperbaric oxygenvasospasmratangiographyArticle30114114612904851Q1WOS:000189304000022Q2