Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 33, Issue 2, Pages 171-174Publisher
SAGE PUBLICATIONS INC
DOI: 10.1038/jcbfm.2012.181
Keywords
A1R; AMP; hypothalamus; hypothermia; stroke
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Funding
- Health Program of the Region of Tuscany
- AstraZeneca
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In light of the relevance of therapeutic hypothermia to stroke treatment, we-investigated whether 5'-adenosine monophosphate (AMP)-dependent cooling affords protection from ischemic brain injury. We show that hypothermia by AMP is because of adenosine A1 receptor. (A1R) activation and is not invariantly associated with hypotension. Inhibition of ecto-5'-nucleotidase-dependent constitutive degradation of brain extracellular AMP by methylene-ADP (AMPCP) also suffices to prompt A1R-dependent hypothermia without hypotension. Both intraischemic and postischemic hypothermia by AMP or AMPCP reduce infarct volumes and mortality of mice subjected to transient middle cerebral artery occlusion. Data disclose that AMP-dependent hypothermia is of therapeutic relevance to treatment of brain ischemia. Journal of Cerebral Blood Flow & Metabolism (2013) 33, 171-174; doi:10.1038/jcbfm.2012.181; published online 5 December 2012
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