Aneurismal subarachnoid haemorrhage (SAH) is a devastating disease that is associated with significant morbidity and mortality. The mortality is approximately 50%, with 30% of survivors having significant morbidity. There is substantial evidence to suggest that oxidative stress is significant in the development of acute brain injury and cerebral vasospasm following SAH. There are several sources for the excessive generation of free radicals following SAH, including disrupted mitochondrial respiration and extracellular hemoglobin. There is also the upregulation of free radical producing enzymes such as inducible nitric oxide synthase (iNOS), xanthine oxidase, NADPH oxidase (NOX), as well as enzymes involved in the metabolism of arachidonic acid. Additionally, intrinsic antioxidant systems such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) are inhibited. Experiments have linked free radicals to the apoptosis of neurons and endothelial cells, BBB breakdown and the altered contractile response of cerebral vessels following SAH. Antioxidant therapy has provided neuroprotection and antispasmotic effects in experimental SAH and some therapies have demonstrated improved outcomes in clinical trials. These studies have laid a foundation for the use of antioxidants in the treatment of aneurismal SAH.

Various reports in the literature have shown that hyperbaric oxygen (HBO) reduces cerebral infarction both in animals and humans. After the initial ischemic insult, however, initiating HBO treatment at different intervals has yielded conflicting results. The present study was undertaken to determine the optimal therapeutic window in which to start HBO treatment for cerebral infarction after transient focal ischemia. In this study, the operator occluded the middle cerebral artery (MCA) of anesthetized rats by introducing a blunted nylon filament into the proximal MCA from the dissected external carotid artery. When the operator removed the filament after 2 h, focal ischemia and reperfusion occurred. The operator then placed the rat in the HBO chamber and administered 3 atm absolute HBO for 1 h according to the protocol. The rat was killed 24 h after reperfusion, and the percentage of infarction (infarct ratio) was calculated by dividing the infarction area by the total area of the ipsilateral hemisphere. The results showed that the percentage of infarcted area decreased significantly (P < 0.05) both in the 3- (7.59%) and 6-h (5.35%) HBO-treatment groups compared with the control (no treatment) group (11.34%). However, the percentage of infarcted area increased significantly (P < 0.01 and P < 0.05, respectively) both in the 12- (23%) and 23-h (20%) treatment groups. The results of this study suggest that applying HBO within 6 h of ischemia-reperfusion injury could benefit the patient but that applying HBO 12 h or more after injury could harm the patient.

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