ArticleExperimental neurology2012
Increased glucose availability does not restore prolonged spreading depression durations in hypotensive rats without brain injury.
Article in Experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Real-time whole-brain imaging of hemodynamics and oxygenation at micro-vessel resolution with ultrafast wide-field photoacoustic microscopy.Light, science & applications · 2022Article
- Requisite ischemia for spreading depolarization occurrence after subarachnoid hemorrhage in rodents.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Large extracellular space leads to neuronal susceptibility to ischemic injury in a Na+/K+ pumps-dependent manner.Journal of computational neuroscience · 2016Article
- Review
- Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature.Physiological reviews · 2015Review
- Dynamics from seconds to hours in Hodgkin-Huxley model with time-dependent ion concentrations and buffer reservoirs.PLoS computational biology · 2014Article
- Subarachnoid hemorrhage, spreading depolarizations and impaired neurovascular coupling.Stroke research and treatment · 2013Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Maintenance of transmembrane ionic gradients and their restoration after cortical spreading depression (CSD) are energy dependent. We recently showed an inverse relationship between blood pressure and CSD duration that is independent of tissue oxygenation. Here, we tested the alternative hypothesis that glucose availability becomes rate-limiting for CSD recovery upon reduced blood pressure in anesthetized rats under full systemic physiological monitoring. Hypotension induced by controlled exsanguination significantly prolonged CSD durations, reduced propagation speeds, and diminished the blood flow response. Hyperglycemia failed to restore the prolonged CSD durations in hypotensive rats and did not significantly alter the propagation speed or the blood flow response. These data suggest that prolonged CSD durations during reduced cerebral perfusion pressure are independent of tissue energy status, and implicate alternative mechanisms of CSD recovery such as vascular clearance of extracellular K(+).
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Registered trials
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