Literature DB >> 22777119

Continuous enteral and parenteral feeding each reduces heart rate variability but differentially influences monocyte gene expression in humans.

Stephen C Gale1, Beth-Ann Shanker, Susette M Coyle, Marie A Macor, Chun W Choi, Steve E Calvano, Siobhan A Corbett, Stephen F Lowry.   

Abstract

Enteral (EN) or parenteral (PN) nutrition is used to support critically ill patients until oral feeding resumes. Enteral nutrition is assumed preferable to PN, but the differential influence on immune function is not well defined. Autonomic nervous activity is known to influence innate immune responses, and we hypothesized that EN and PN could influence both autonomic signaling and gene activation in peripheral blood monocytes (PBMs). Ten subjects (aged 18-36 years) received continuous EN or PN for 72 h. Peripheral blood monocytes were isolated from whole blood before and after continuous feeding and were analyzed for gene expression using a microarray platform. Gene expression after feeding was compared from baseline and between groups. To measure autonomic outflow, subjects also underwent heart rate variability (HRV) monitoring during feeding. Time and frequency domain HRV data were compared between groups and five orally fed subjects for changes from baseline and changes over time. During continuous EN and PN, subjects exhibited declines in both time and frequency domain HRV parameters compared with baseline and with PO subjects, indicating a loss of vagal/parasympathetic tone. However, PN feeding had a much greater influence on PBM gene expression compared with baseline than EN, including genes important to innate immunity. Continuous EN and PN are both associated with decreasing vagal tone over time, yet contribute differently to PBM gene expression, in humans. These preliminary findings support assumptions that PN imposes a systemic inflammatory risk but also imply that continuous feeding, independent of route, may impart additional risk through different mechanisms.

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Year:  2012        PMID: 22777119      PMCID: PMC3428199          DOI: 10.1097/SHK.0b013e31826171b9

Source DB:  PubMed          Journal:  Shock        ISSN: 1073-2322            Impact factor:   3.454


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