Central autonomic network mediates cardiovascular responses to acute inflammation: relevance to increased cardiovascular risk in depression?

Harrison, Neil, Cooper, Ella, Voon, Valerie, Miles, Kenneth Alan and Critchley, Hugo (2013) Central autonomic network mediates cardiovascular responses to acute inflammation: relevance to increased cardiovascular risk in depression? Brain, behavior, and immunity, 31. pp. 189-196. ISSN 1090-2139

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Abstract

Inflammation is a risk factor for both depression and cardiovascular disease. Depressed mood is also a cardiovascular risk factor. To date, research into mechanisms through which inflammation impacts cardiovascular health rarely takes into account central effects on autonomic cardiovascular control, instead emphasizing direct effects of peripheral inflammatory responses on endothelial reactivity and myocardial function. However, brain responses to inflammation engage neural systems for motivational and homeostatic control and are expressed through depressed mood state and changes in autonomic cardiovascular regulation. Here we combined an inflammatory challenge, known to evoke an acute reduction in mood, with neuroimaging to identify the functional brain substrates underlying potentially detrimental changes in autonomic cardiovascular control. We first demonstrated that alterations in the balance of low to high frequency (LF/HF) changes in heart rate variability (a measure of baroreflex sensitivity) could account for some of the inflammation-evoked changes in diastolic blood pressure, indicating a central (rather than solely local endothelial) origin. Accompanying alterations in regional brain metabolism (measured using (18)FDG-PET) were analysed to localise central mechanisms of inflammation-induced changes in cardiovascular state: three discrete regions previously implicated in stressor-evoked blood pressure reactivity, the dorsal anterior and posterior cingulate and pons, strongly mediated the relationship between inflammation and blood pressure. Moreover, activity changes within each region predicted the inflammation-induced shift in LF/HF balance. These data are consistent with a centrally-driven component originating within brain areas supporting stressor evoked blood pressure reactivity. Together our findings highlight mechanisms binding psychological and physiological well-being and their perturbation by peripheral inflammation.

Item Type: Article
Schools and Departments: Brighton and Sussex Medical School > Clinical Medicine
Brighton and Sussex Medical School > Neuroscience
Subjects: R Medicine > R Medicine (General) > R895 Medical physics. Medical radiology. Nuclear medicine
R Medicine > RC Internal medicine > RC0321 Neurosciences. Biological psychiatry. Neuropsychiatry
Depositing User: Hazelle Woodhurst
Date Deposited: 06 Aug 2014 08:44
Last Modified: 27 Jul 2017 18:06
URI: http://sro.sussex.ac.uk/id/eprint/49493
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