Disturbed microcirculation and hyperaemic response in a murine model of systemic inflammation

Area of Science:

• Neuroscience
• Immunology
• Cerebrovascular biology

Background:

• Systemic inflammation is linked to cognitive impairment and dementia risk.
• Cytokines mediate inflammation's effects on neurons, potentially causing neurodegeneration with prolonged exposure.
• The impact of systemic inflammation on cerebral vasculature and brain oxygenation is not well understood.

Purpose of the Study:

• To investigate the effects of acute systemic inflammation on neurovascular coupling in mice.
• To examine alterations in cerebral blood flow and capillary function during inflammation.

Main Methods:

• Lipopolysaccharide (LPS) was administered to induce systemic inflammation in awake mice.
• Pial vessel responses to functional activation were measured.
• Capillary blood flow dynamics and 'capillary stalls' were analyzed under steady-state conditions.

Main Results:

• LPS-induced inflammation significantly attenuated and delayed the hyperaemic response of pial vessels to functional activation.
• A notable increase in blocked capillaries and prolonged 'capillary stalls' was observed.
• These vascular changes indicate impaired blood flow and oxygen delivery to the brain.

Conclusions:

• Acute systemic inflammation profoundly disturbs neurovascular coupling.
• Impaired cerebral oxygen availability due to vascular changes may underlie cognitive deficits.
• These findings suggest a potential mechanism linking acute inflammation to chronic neurodegenerative processes and dementia risk.