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Ischemic Preconditioning Attenuates Brain Edema After Experimental Intracerebral Hemorrhage

Translational Stroke Research : Volume 3, Issue 2, June 2012

Translational Stroke Research : Volume 3, Issue 1, March 2012

Translational Stroke Research : Volume 2

Translational Stroke Research : Volume 1

Ischemic Preconditioning Attenuates Brain Edema After Experimental Intracerebral Hemorrhage

Content Provider	Springer Nature Link
Author	He, Yangdong Karabiyikoglu, Murat Hua, Ya Keep, Richard F. Xi, Guohua
Copyright Year	2012
Abstract	Ischemic preconditioning (IPC) provides protection against subsequent severe ischemic injury. A recent study found that cerebral IPC prolongs bleeding time. In this study, we examined whether IPC protects against intracerebral hemorrhage (ICH)-induced brain edema formation and whether IPC affects blood coagulation. There were three sets of experiments in this study. In the first set, male Sprague–Dawley rats were preconditioned with either 15 min of left middle cerebral artery occlusion, an IPC stimulus, or a sham operation. Three days later, rats received an infusion of autologous whole blood in the ipsilateral or contralateral caudate. Rats were killed 24 h later for brain water content measurement. In the second set, rats underwent 15 min of IPC or a sham operation. Three days later, rats were used for bleeding and thrombin clotting time tests. In the third set, the levels of p44/42 mitogen-activated protein kinases (MAPKs), heme oxygenase-1 (HO-1), transferrin (Tf), and transferrin receptor (TfR) in the brain 24 or 72 h after IPC were examined. We found that IPC reduced ICH-induced brain edema when blood was injected into the ipsilateral caudate but it did not when blood was injected into the contralateral caudate. IPC resulted in prolongation of bleeding time and thrombin clotting time. IPC also induced the activation of p44/42 MAPKs and upregulation of HO-1, Tf, and TfR levels in the ipsilateral caudate. These results suggest that IPC protects against ICH-induced brain edema formation and decreases blood coagulation. The protection of IPC against ICH is mainly due to local factors in the brain and may be related to activation of p44/42 MAPKs and upregulation of HO-1, Tf, and TfR.
Starting Page	180
Ending Page	187
Page Count	8
File Format	PDF
ISSN	18684483
Journal	Translational Stroke Research
Volume Number	3
Issue Number	1
e-ISSN	1868601X
Language	English
Publisher	Springer-Verlag
Publisher Date	2012-04-17
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Brain edema Ischemic preconditioning p44/42 mitogen activated protein kinases Heme oxygenase-1 Transferrin Transferrin receptor Intracerebral hemorrhage Neurosurgery Cardiology Vascular Surgery Neurosciences Neurology
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine Neuroscience Neurology (clinical)

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