| Project/Area Number |
11680862
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biomedical engineering/Biological material science
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| Research Institution | Kochi Medical School (2000-2001)
National Cardiovascular Center Research Institute (1999) |
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Principal Investigator |
SATO Takayuki Kochi Medical School, Medicine, Professor, 医学部, 教授 (90205930)
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| Co-Investigator(Kenkyū-buntansha) |
RAICU Valerica Kochi Medical School, Medicine, Instructor, 医学部, 助手 (20304678)
KAWADA Toru National Cardiovascular Center Research Institute, Cardiovascular Dynamics, Instructor, 循環動態機能部, 室員 (30243752)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | arterial baroreflex / Shy-Drager syndrome / dynamics / sympathetic nerve / orthostatic hypotension / bionics / systems physiology |
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| Research Abstract |
Background : We developed a bionic technology for the treatment of baroreflex failure, and tested its efficacy in restoration of arterial pressure against head-up tilt (HUT) in rats with baroreflex failure.
Methods and Results : The bionic baroreflex system (BBS) was a negative feedback system controlled by a computer, the artificial vasomotor center. It sensed systemic arterial pressure (SAP) through a micromanometer placed in the aortic arch and automatically computed the frequency of a pulse train to stimulate sympathetic efferent nerves. We selected the celiac ganglion as the sympathetic vasomotor interface for the BBS, because the abdominal vascular bed innervated by the greater splanchnic nerve is a major effector mechanism for the baroreflex control of arterial pressure. To make this system to be BIONIC, the operational rule of the artificial vasomotor center (H_<BRP→STM>) was actively matched to that of the native center. First, we identified the open-loop transfer functions of the native baroreflex control of SAP (H_<Native>) and the response of SAP to electrical stimulation of the celiac ganglion (H_<STM→SAP>). We computed H_<BRP→STM> from H_<Native>/H_<STM→SAP>, and transplanted the operational rule into the computer. In 10 rats with baroreflex failure, we evaluated the performance of the BBS during rapid hypotension induced by HUT. Abrupt head-up tilting dropped SAP by 34±6 mmHg in 2 sec, and by 52±5 mmHg in 10 sec. During real-time execution of the BBS, on the other hand, the fall in SAP was 21±5 mmHg at 2 sec, and 15±6 mmHg at 10 sec after HUT. These arterial responses controlled by the BBS were indistinguishable from those by the native baroreflex.
Conclusions : We concluded that the BBS revitalized the native baroreflex function in rats with baroreflex failure.
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