ReviewJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2011
α(2)-adrenoceptors do not mediate neuroprotection in acute ischemic stroke in mice.
Review in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Method parameters' impact on mortality and variability in mouse stroke experiments: a meta-analysis.Scientific reports · 2016Pooled it
- Effects of precondition αNaunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Adrenergic receptor antagonism induces neuroprotection and facilitates recovery from acute ischemic stroke.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- A diseasome cluster-based drug repurposing of soluble guanylate cyclase activators from smooth muscle relaxation to direct neuroprotection.NPJ systems biology and applications · 2018Article
- Bombesin-like receptor 3 regulates blood pressure and heart rate via a central sympathetic mechanism.American journal of physiology. Heart and circulatory physiology · 2016Article
- The two-pore domain potassium channel KCNK5 deteriorates outcome in ischemic neurodegeneration.Pflugers Archiv : European journal of physiology · 2015Review
- Neuroprotection for stroke: current status and future perspectives.International journal of molecular sciences · 2012Review
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
We assessed the neuroprotective potential of α(2)-adrenoceptors in ischemic stroke using mice with targeted deletions of individual α(2)-adrenoceptor subtypes (α(2A)(-/-), α(2B)(-/-), α(2C)(-/-), α(2A/C)(-/-)). The effects of the α(2)-adrenoceptor agonist clonidine were studied in parallel. Focal cerebral ischemia was induced with or without clonidine pretreatment by transient middle cerebral artery occlusion. Neurologic outcome and infarct volumes were evaluated on day 1. Cerebral blood flow (CBF) and mean arterial pressure were determined. α(2)-Adrenoceptor null mice did not display larger infarct volumes compared with wild-type (WT) mice under basal conditions (P>0.05). In line with this finding, pretreatment with clonidine did not protect from ischemic brain damage in WT mice or α(2A)(-/-), α(2B)(-/-), and α(2C)(-/-) mice. Clonidine induced smaller infarct volumes only in α(2A/C)(-/-) mice (P<0.05), but this did not translate into improved neurologic function (P>0.05). Importantly, while clonidine caused a significant decrease in arterial blood pressure in all groups, it had no blood pressure lowering effect in α(2A/C)(-/-) mice, and this correlated with higher CBF and smaller infarct volumes in this group. In summary, we could not demonstrate a neuroprotective function of α(2)-adrenoceptors in focal cerebral ischemia. Careful controlling of physiological parameters relevant for stroke outcome is recommended in experimental stroke studies.
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