Analysis of central mechanism of hypoxic respiratory inhibition
| Project/Area Number |
01570039
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General physiology
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| Research Institution | Chiba University |
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Principal Investigator |
FUKUDA Yasuichiro Chiba University, SCH. MED. Assoc. Professor, 医学部, 助教授 (10009649)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1990: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1989: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Hypoxia / Respiratory center / Respiratory inhibition / Blood pressure / Peripheral chemoreceptor / Sympathetic nervous activity / Cardiac output / Metabolic rate / 酸素消費量 / 呼吸調節 / 炭酸ガス / ラット |
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| Research Abstract |
Central mechanism of respiratory inhibition during acute severe hypoxia was investigated in the anesthetized rat. Circulatory variables and autonomic nervous activities as well as changes in ventilatory parameters were measured.
In the carotid sinus nerve (CSN) intact rats, ventilatory augmentation was followed by depression due to reduction in respiratory frequency (f) at end-tidal Po_2 levels below 50-60 mmHg despite increased afferent activities from the carotid chemoreceptors. After CSN section, ventilation was progressively depressed at and-tidal Po_2 lower than normoxic level with simultaneous decreases of f and tidal volume. An increase in CO_2 stimulus or the prevention of arterial hypotension during hypoxia by infusing a vasoconstrictor agent (phenylephrine) inhibited the occurrence of ventilatory depression in both the CSN intact and denervated animals. In all cases studied, the reduction in f resulted mainly from the selective prolongation of expiratory time. The results sugg
… More
est that in the anesthetized rat the effect of respiratory stimulation from carotid chemoreceptor afferents becomes inadequate to offset the prolongation of expiratory time due to the central hypoxia at lower end-tidal Po_2, and that the neural process for regulating expiratory time is the major site of deterioration during central hypoxic inhibition. The reduction in sympathetic nervous activity and a direct hypoxic vasodilatation resulted in profound hypotension during severe hypoxia.
Hypoxic respiratory inhibition was accompanied by reduction in cardiac output and metabolic rate (oxygen consumption). During the breathing of normoxic air, oxygen consumption was fairly constant, independent of a wide variation of cardiac output, whereas in hypoxia by respiratory inhibition was induced, oxygen consumption was closely dependent upon cardiac output or the rate of oxygen delivery to tissue. Combined respiratory, circulatory and flow dependent metabolic inhibition may represent an integrative response process against oxygen shortage.
Hypoxic respiratory inhibition was effectively attenuated by chronic administration of either progestin or a substance which increases the hemoglobin-oxygen affinity. Less
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Report
(3 results)
Research Products
(21 results)
