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Systemic inflammation affects reperfusion following transient cerebral ischaemia
F Burrows1, M J Haley1, E Scott1
1Faculty of Life Sciences, The University of Manchester, Stopford Building, Oxford Road, M13 9PT Manchester, UK.
Experimental Neurology
|January 23, 2016
Summary
Systemic inflammation worsens stroke outcomes by causing the no-reflow phenomenon, reducing blood flow recovery. Anti-inflammatory treatments may improve reperfusion after ischemic stroke.
Area of Science:
- Neuroscience
- Immunology
- Vascular Biology
Background:
- Reperfusion therapies for stroke, such as recombinant tissue plasminogen activator and endovascular intervention, are limited to a small patient subset.
- The no-reflow phenomenon, characterized by inadequate microvascular reperfusion, significantly hinders stroke recovery and patient survival.
- Emerging evidence implicates systemic inflammation as a key factor contributing to the no-reflow phenomenon.
Purpose of the Study:
- To investigate the role of systemic inflammation, specifically interleukin-1 (IL-1), in exacerbating the no-reflow phenomenon following ischemic stroke.
- To analyze the impact of IL-1 on microvascular perfusion, platelet aggregation, and neuropathological markers in a mouse model of stroke.
Main Methods:
- Mice were administered interleukin-1 (IL-1) intraperitoneally 30 minutes prior to middle cerebral artery (MCA) occlusion to induce focal ischemia.
- Two-dimensional optical imaging spectroscopy was employed to monitor spatiotemporal dynamics of oxyhemoglobin concentration in the MCA-perfused cortical area.
- Post-reperfusion analysis included CD41 immunohistochemistry for platelet aggregation, assessment of microglial activation (IL-1α), blood-brain barrier integrity (IgG infiltration), and neuronal damage (pyknotic changes).
Main Results:
- Systemic inflammation induced by IL-1 significantly reduced oxyhemoglobin reperfusion as early as 3 hours post-reperfusion compared to vehicle-treated controls.
- Increased hyper-coagulated platelets were observed within the microvasculature of the stroked cortex in the IL-1 group.
- Elevated markers of ischemic damage, including microglial activation, blood-brain barrier breakdown, and neuronal pyknosis, were evident in IL-1 treated mice.
Conclusions:
- Systemic inflammation is a significant contributor to the no-reflow phenomenon in the post-ischemic brain.
- Targeting inflammatory pathways with anti-inflammatory approaches may represent a promising therapeutic strategy to improve reperfusion and outcomes in ischemic stroke patients.
Keywords:
Co-morbidityInterleukin-1Interleukin-1βMiddle cerebral artery occlusionOptical imagingReperfusionSpectroscopyStrokeSystemic inflammationMore Related Videos
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