In silico study of the influence of intensity and duration of blood flow reduction on cell death through necrosis or apoptosis during acute ischemic stroke

Abstract : Ischemic stroke involves numerous and complex pathophysiological mechanisms including blood flow reduction, ionic exchanges, spreading depressions and cell death through necrosis or apoptosis. We used a mathematical model based on these phenomena to study the influences of intensity and duration of ischemia on the final size of the infarcted area. This model relies on a set of ordinary and partial differential equations. After a sensibility study, the model was used to carry out in silico experiments in various ischemic conditions. The simulation results show that the proportion of apoptotic cells increases when the intensity of ischemia decreases, which contributes to the model validation. The simulation results also show that the influence of ischemia duration on the infarct size is more complicated. They suggest that reperfusion is beneficial when performed in the early stroke but may be either inefficacious or even deleterious when performed later after the stroke onset. This aggravation could be explained by the depolarisation waves which might continue to spread ischemic damage and by the speeding up of the apoptotic process leading to cell death. The effect of reperfusion on cell death through these two phenomena needs to be further studied in order to develop new therapeutic strategies for stroke patients.
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Article dans une revue
Acta Biotheoretica, Springer Verlag, 2010, 58 (2-3), pp.171-190. 〈10.1007/s10441-010-9100-2〉
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Contributeur : Emmanuel Grenier <>
Soumis le : vendredi 15 février 2013 - 10:04:35
Dernière modification le : jeudi 18 janvier 2018 - 01:39:09

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Guillemette Chapuisat, Marie-Aimée Dronne, Emmanuel Grenier, Marc Hommel, Jean-Pierre Boissel. In silico study of the influence of intensity and duration of blood flow reduction on cell death through necrosis or apoptosis during acute ischemic stroke. Acta Biotheoretica, Springer Verlag, 2010, 58 (2-3), pp.171-190. 〈10.1007/s10441-010-9100-2〉. 〈hal-00788715〉

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