• Zhiyong Qin, Murat Karabiyikoglu, Ya Hua, Robert Silbergleit, Yangdong He, Richard F Keep, and Guohua Xi.
• Department of Neurosurgery, University of Michigan, Ann Arbor, MI 48109-2200, USA.
• Stroke. 2007 Apr 1; 38 (4): 1362-7.

Background And PurposeAn increased risk of hemorrhagic transformation is a major factor limiting the use of tissue plasminogen activator for stroke. Increased hemorrhagic transformation is also found in animals undergoing transient focal cerebral ischemia with hyperglycemia; this study examined whether hyperbaric oxygen (HBO) could reduce such hemorrhagic transformation in a rat model.MethodsRats received an injection of 50% glucose (6 mL/kg intraperitoneally) and had a middle cerebral artery occlusion 10 minutes later. Rats were treated with HBO (3 ATA for 1 hour) 30 minutes after middle cerebral artery occlusion. Control rats received normobaric room air. Rats underwent reperfusion 2 hours after middle cerebral artery occlusion. Blood-brain barrier permeability (Evans blue), hemorrhagic transformation (hemoglobin content), brain edema, infarct volume, and mortality were measured.ResultsHBO treatment reduced Evans blue leakage in the ipsilateral hemisphere (28.4+/-3.5 versus 71.8+/-13.1 microg/g in control group, P<0.01) 2 hours after reperfusion and hemorrhagic transformation (0.13+/-0.13 versus 0.31+/-0.28 mg hemoglobin in the control group, P<0.05) 22 hours later. Mortality was less in the HBO group (4% versus 27% in controls, P<0.05). Mean infarct volume and swelling in the caudate were also less in HBO-treated rats (P<0.05), but HBO failed to reduce brain water content in the ipsilateral hemisphere (P>0.05).ConclusionsEarly intraischemic HBO treatment reduces the blood-brain barrier disruption, hemorrhagic transformation, and mortality after focal cerebral ischemia suggesting that HBO could be used to reduce hemorrhagic conversion in patients with stroke.

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