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Hypovolemia affects cortical activity patterns associated with the cardiovascular response to moderate lower body negative pressure (LBNP)
Author(s) -
Usselman Charlotte Willemina,
Wong Savio W,
Kimmerly Derek S,
Rothwell Amanda,
Shoemaker J Kevin
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.740.15
Subject(s) - baroreceptor , hypovolemia , baroreflex , medicine , blood oxygen level dependent , hippocampal formation , cardiology , thalamus , putamen , neuroscience , functional magnetic resonance imaging , blood pressure , heart rate , psychology
We tested the hypothesis that hypovolemia (HV; reduced blood volume) modifies the cortical autonomic network (CAN) response to moderate (−35 mmHg) LBNP. CAN activity was assessed using functional magnetic resonance imaging (fMRI) with blood oxygen level‐dependent (BOLD) contrast in young healthy subjects (n = 9). Testing was repeated under normovolemia (NV) and HV (spironolactone: 100mg/day for 3 days; randomized). BOLD data were collected at baseline and during 3 repeated 60s bouts of LBNP (separated by 90s rest periods). Random effects analysis revealed BOLD signal changes (p < 0.005, uncorrected) in the CAN during both the onset (baroreceptor unloading) and offset (baroreceptor loading) phases of LBNP. In both NV and HV, LBNP onset induced CAN BOLD signal changes in the thalamus, hippocampus, putamen, mid‐cingulate cortex and posterior insular cortex. In addition, LBNP onset in HV also elicited BOLD signal changes in the caudate nucleus, and anterior and posterior cingulate cortex. Changes in these additional areas were observed again during HV offset, although HV offset did not elicit a change in hippocampal activation. Compared to NV, these results suggest that HV was associated with more widespread CAN activation during the dynamic phases of baroreceptor manipulation. Supported by the Canadian Space Agency.