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Hyperglycemia and Hemorrhagic Transformation of Cerebral Infarction: A Macroscopic Hemorrhagic Transformation Rat Model

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Intracerebral Hemorrhage Research

Part of the book series: Acta Neurochirurgica Supplementum ((NEUROCHIRURGICA,volume 111))

Abstract

The recombinant tissue plasminogen activator (t-PA) is a useful therapy for acute ischemic stroke patients, but there is a major risk factor of hemorrhagic transformation. Hyperglycemic patients are not able to admit t-PA because hyperglycemia exaggerates ischemic brain and vascular damage following transient focal cerebral ischemia and frequently induces hemorrhagic transformation of the infarct during reperfusion. However, the mechanisms underlying hemorrhagic transformation induced by hyperglycemia are still unknown. Furthermore, previous reports focused upon microscopic hemorrhage rather than macroscopic hemorrhagic transformation. In order to make these problems clear, it is necessary to establish an experimental model that induces constant macroscopic hemorrhagic transformation in the infarct area caused by middle cerebral artery occlusion and the reperfusion model on the hyperglycemic rat. This experimental study can establish the model in which macroscopic hemorrhagic transformation occurs following 1.5 h occlusion and 24 h reperfusion by using the intraluminal thread method on hyperglycemic rats. It might be useful to determine the mechanisms and understand why hyperglycemia exaggerates the causes inducing macroscopic hemorrhagic transformation in the infarct area, and this reproducible model provides a platform for evaluating treatment strategies.

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Correspondence to Tamiji Tsubokawa .

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© 2011 Springer-Verlag/Wien

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Tsubokawa, T., Joshita, H., Shiokawa, Y., Miyazaki, H. (2011). Hyperglycemia and Hemorrhagic Transformation of Cerebral Infarction: A Macroscopic Hemorrhagic Transformation Rat Model. In: Zhang, J., Colohan, A. (eds) Intracerebral Hemorrhage Research. Acta Neurochirurgica Supplementum, vol 111. Springer, Vienna. https://doi.org/10.1007/978-3-7091-0693-8_8

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  • DOI: https://doi.org/10.1007/978-3-7091-0693-8_8

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  • Publisher Name: Springer, Vienna

  • Print ISBN: 978-3-7091-0692-1

  • Online ISBN: 978-3-7091-0693-8

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