ID | 32869 |
JaLCDOI | |
FullText URL | |
Author |
Tanakaya, Machiko
Takahashi, Natsuki
Takeuchi, Kazufumi
Katayama, Yusuke
Yumoto, Akihisa
Kohno, Kunihisa
Shiraki, Teruo
Saito, Daiji
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Abstract | Postprandial hypotension is an important hemodynamic abnormality in diabetes mellitus, but few reports are available on the relationship between autonomic dysfunction and postprandial hypotension. Ten diabetic patients and 10 healthy volunteers were recruited for this study. Postural blood pressure and heart rate changes were measured before lunch, and then the hemodynamic responses to a standardized meal were investigated. Holter electrocardiogram (ECG) monitoring was conducted for assessing spectral powers and time-domain parameters of RR variations. Postural changes from the supine to the upright position decreased the systolic blood pressure of the diabetics from 133(+-)16 to 107(+-)20 mmHg (p<0.01), but did not decrease the systolic blood pressure of the controls. The heart rate remained constant in the diabetics but was increased in the controls. Food ingestion decreased systolic blood pressure in the diabetics, with a maximum reduction of 25(+-)5 mmHg. This decrease was not associated with any changes in the ratio of low frequency to high frequency, and yet the heart rate remained almost constant. Indexes involving parasympathetic tone were not affected. Food ingestion did not affect blood pressure in the control group. These findings suggest that lack of compensatory sympathetic activation is a factor contributing to postprandial hypotension in diabetics, and that parasympathetic drive does not make a significant contribution to this condition.
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Keywords | postprandial hypotension
sympathetic tone
RR variability
diabetes mellitus
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Amo Type | Original Article
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Publication Title |
Acta Medica Okayama
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Published Date | 2007-08
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Volume | volume61
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Issue | issue4
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Publisher | Okayama University Medical School
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Start Page | 191
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End Page | 197
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ISSN | 0386-300X
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NCID | AA00508441
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Content Type |
Journal Article
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language |
English
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File Version | publisher
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Refereed |
True
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PubMed ID | |
Web of Science KeyUT |