Post-stroke sleep apnea: the effect of intermittent hypoxia on cerebrovascular recovery

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Introduction: Ischemic stroke is the death of brain cells due to lack of oxygen caused by blockage of blood flow. Stroke is associated with decline in cognitive function. The cerebrovascular recovery process can be complicated by certain comorbidities, including obstructive sleep apnea syndrome (OSA). This syndrome affects nearly 50% of post-stroke patients. We conducted a preclinical study in rats to decipher the pathophysiological mechanisms of the stroke-OSA interaction. Methods: Rats were submitted to an experimental stroke model with malonate injection (2ul,3M) followed by exposure to Intermittent hypoxia (IH group) or normoxia (N group) from 4 to 56 days. We characterized brain lesion size and microvascular plasticity using in vivo microvascular 4.7T-MRI along with qPCR and immunohistological analysis. Results: In MRI, lesion size was not significantly affected by IH compared to N. IH increased vessel size and blood volume at D04 and D28, and increased blood brain barrier leakage at D04. Immuno-histological analysis showed that at D28 IH increased GFAP and ColIV and decreased NeuN with no effect on ZO-1. Molecular analysis showed that IH increased VEGF, VEGFR1 and VEGFR2 gene expression at D07 but decreased them along at D28. Finally, IH increased gene expression of inflammatory molecules IL6 (D07 and D28) and TGF-B and TNF-alpha (D07). It also decreased SOD1 at D04 and D28. IH had no effect on catalase, Ang1, Ang2, Nrf1, HIF-1 and NF-KB. Conclusion: IH moderately affects ischemic injury recovery in a time dependent matter by altering inflammation, oxidative stress and brain vasculature. Future studies should investigate the clinical implications for post-stroke sleep apnea patients.

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