| Summary: | Heart Failure (HF) is a devastating disease with an increasing incidence that is associated with multiple comorbidities. Cognitive impairment (CI) is one of the most common coexisting chronic conditions in HF. Despite this strong association, the underlying pathophysiological mechanisms remain unknown, especially in HF with Preserved Ejection Fraction (HFpEF).
We evaluated the effects of HFpEF on microglia and astrocyte activation and neuroinflammation in the hippocampal formation, a fundamental brain region in cognitive functions.
The study was conducted on ZSF1‐Lean and ZSF1‐Obese rats, a metabolic risk-related HFpEF animal model. Animals were evaluated periodically through echocardiography. The numerical density of GFAP- and CD11b-immunoreactive cells in hippocampal formation were estimated using stereological procedures. Cytokine mRNA relative expression was measured.
30 week-old ZSF1-Obese rats showed an elevated left ventricular (LV) end-diastolic pressure, a higher LV mass and a higher E/E' ratio than ZSF1-Lean rats but similar ejection fraction, confirming the cardiac HFpEF phenotype in ZSF1-Obese rats. The numerical density of GFAP- and CD11b-positive cells in all of the hippocampal formation subfields were identical between groups. Although ZSF1-Obese and ZSF1-Lean rats showed no significant differences in IL-1β, IL-6 and COX-2 gene expression, expression of TNF-α was significantly increased in ZSF1-Obese rats.
Our results suggest that in ZSF1‐Obese rats, an experimental model of HFpEF, there is no induction of microglial or astrocyte activation in the hippocampal formation, although there was a glial shift towards a pro-inflammatory phenotype.
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