1996 Fiscal Year Final Research Report Summary
Cardiorespiratory outputs during sleep-simulated state in animal models
| Project/Area Number |
07670656
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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 |
Respiratory organ internal medicine
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| Research Institution | Chiba University |
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Principal Investigator |
KIMURA Hiroshi Chiba University School of Medicine Associate Professor, 医学部, 助教授 (20195374)
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| Co-Investigator(Kenkyū-buntansha) |
TATSUMI Koichiro Chiba University Hospital, Assistant, 医学部・附属病院, 助手 (10207061)
HAYASHI Fumiaki Chiba University School of Medicine Lecturer, 医学部, 講師 (80173029)
FUKUDA Yasuichiro Chiba University School of Medicine Professor, 医学部, 教授 (10009649)
KURIYAM Takayuki Chiba University School of Medicine Professor, 医学部, 教授 (20009723)
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| Project Period (FY) |
1995 – 1996
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| Keywords | OBSTRUCTIVE SLEEP APNEA / REM SLEEP / HYPOXIA / PULMONARY ARTERIAL PRESSURE / INTERCOSTAL MUSCLES / PERIPHERAL CHEMORECEPTORS / ELECTROMYOGRAM |
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| Research Abstract |
Several issues on the deterioration of cardiorespiratory outputs during sleep were analyzed to investigate the pathogenesis of sleep-related disorders. As the pathophysiological mechanisms to cause sleep-related disorders are thought to be manifold, we tried to study from various kinds of views : from animal models to patients with sleep apnea syndrome. As to the central mechanism to cause respiratory depression during REM sleep, the role of disfacilitation from the respiratory center was well investigated. Based on these observations, we have investigated how afferent signals arising from peripheral chemoreceptors modulate pulmonary arterial pressure (PAP) elevation during hypoxic exposure in rats which was simulating sleep apnea. Although hypoxia elicited an increase in PAP that is mainly determined by hypoxic pulmonary vasoconstriction, central inputs from peripheral chemoreceptors, probably through the autonomic nervous system, could also affect the PAP changes during the hypoxic exposure. In this study, it is concluded that intact peripheral chemoreceptors are necessary for PAP elevation in response to hypoxia. Furthermore, we have studied on the neuromuscular control of upper airway dilating muscle during acute hypoxia in patients with obstructive sleep apnea syndrome (OSAS). The hypoxic response of genioglossal muscle activity (GG) as compared with that of diaphragm was activated to more extent in OSAS than in normal control. We previously reported that hypoxic depression in GG was more prominent as compared to that of diaphragm in OSAS than in normal control. Taken together, we conclude that the adaptation process to hypoxia might play a role, at least in part, in producing the deterioration of the upper airway muscle activity during sleep.
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