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Updated: Jul 16, 2026

A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia
Published on: November 15, 2024
Hyperbaric oxygen-induced attenuation of hemorrhagic transformation after experimental focal transient cerebral
Zhiyong Qin1, Murat Karabiyikoglu, Ya Hua
1Department of Neurosurgery, University of Michigan, Ann Arbor, MI 48109-2200, USA.
Background And Purpose:
An 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.
Methods:
Rats 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.
Results:
HBO 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).
Conclusions:
Early 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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