ArticleJournal of molecular neuroscience : MN2015
Scheme of Ischaemia-triggered Agents during Brain Infarct Evolution in a Rat Model of Permanent Focal Ischaemia.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 7 citations in OpenAlex.
- Brain to blood efflux as a mechanism underlying the neuroprotection mediated by rapid remote preconditioning in brain ischemia.Molecular biology reports · 2020Article
- Time-course investigation of blood-brain barrier permeability and tight junction protein changes in a rat model of permanent focal ischemia.The journal of physiological sciences : JPS · 2018Article
- Chronic stress induced disruption of the peri-infarct neurovascular unit following experimentally induced photothrombotic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The impact of therapeutic intervention in stroke depends on its appropriate timing during infarct evolution. We have studied markers of brain tissue damage initiated by permanent occlusion of the middle cerebral artery (MCAO) at three time points during which the infarct spread (1, 3 and 6 h). Based on Evans Blue extravasation and immunohistochemical detection of neurons, we confirmed continuous disruption of blood-brain barrier and loss of neurons in the ischaemic hemisphere that peaked at the sixth hour, especially in the core. Glutamate content started to rise dramatically in the entire hemisphere during the first 3 h; the highest level was determined in the core 6 h after MCAO (141 % increase). Moreover, the enzyme antioxidant defence grew by about 42 % since the first hour in the ipsilateral penumbra. Enzymes of the apoptotic pathway as well as mitochondrial enzyme release were detected since the third hour of MCAO in the ischaemic hemisphere; all achieved their maxima in the penumbra during both time periods (except cytochrome C). In conclusion, the preserved integrity of mitochondrial membrane and incompletely developed process of apoptosis may contribute to the better therapeutic outcome after ischaemic attack; however, a whole brain response should not be omitted.
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