1996 Fiscal Year Final Research Report Summary
Mechanisms of the reflexive respiratory suppression induced by thin-fiber muscular afferents under low O2 and high CO2 environments.
| Project/Area Number |
07457017
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | Research Institute of Environmental Medicine, Nagoya University |
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Principal Investigator |
KOZAKI Yasuko Res. Inst. Environ. Med., Nagoya Univ. Research Associate, 環境医学研究所, 助手 (20126882)
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| Co-Investigator(Kenkyū-buntansha) |
KUMAZAWA Takao Res. Inst. Environ. Med., Nagoya Univ. Professor Emeritus, 名誉教授 (20022775)
KASAI Masanori Res. Inst. Environ. Med., Nagoya Univ. Assistant Professor, 環境医学研究所, 助手 (30202005)
MIZUMURA Kazue Res. Inst. Environ. Med., Nagoya Univ. Professor, 環境医学研究所, 教授 (00109349)
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| Project Period (FY) |
1995 – 1996
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| Keywords | respiration / reflexive respiratory suppression / noxious input / hypoxia / hypercapnia / beta-endorphin / morphine |
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| Research Abstract |
Present study evaluated influences of noxious gas-environment on respiratory negative feedback induced by nociceptive input. In anesthetized, artificially ventilated cats in which arterial gas tensions were continuously monitored, respiratory response to electrical stimulation of thin-fiber muscular afferents was studied at different levels of respiration induced by different gas tensions. Respiratory outputs was estimated from phrenic nerve discharges and standardized by the first inflection point (standard point) of CO<@D22@>D2 response curve of individual cat. The respiration at the standard point is conveniently referred to as control level. At the augmented levels of respiration by low O<@D22@>D2 (end-expiratory 10.0(]SY.+-。[)0.4%, n=4) or high CO<@D22@>D2 tension (end-expiratory 6.0(]SY.+-。[)0.3%, n=10) the magnitudes of the reflexive respiratory suppression were attenuated, compared with those at the control level (end-expiratory CO<@D22@>D2 : 4.3(]SY.+-。[)0.2%, O<@D22@>D2 : 20.
… More
5(]SY.+-。[)0.3%, respectively). Thus it is considered that the facilitatory component of the augmented pre-stimulus level of respiration overcome the inhibitory component induced by excessive afferent input.
The reflexive respiratory suppression is thought to be mediated by endogenous opioidergic system. We measured beta-endorphine in cerebrospinal perfusate of caudal part of brainstem region, which is known to control respiratory function. Noxious gas-environment (inhalation of either 8 % O_2 (n=5) or 6 % CO_2 (=5)) did not induce any consistent changes in beta-endorphine-like immunoreactivities measured by ELISA.
At the augmented levels of respiration by high CO<@D22@>D2 tension (end-expiratory 6.0(]SY.+-。[)0.4 %, n=6) the magnitudes of the respiratory depression induced by morphine (i. v.) tended to decrease, compared with those at control level (end-expiratory 4.7(]SY.+-。[)0.4 %, n=6). This result would mean that the facilitatory component of the augmented pre-stimulus level of respiration overcame the inhibitory component induced by administration of exogenous opioid, as suggested for the reflexive respiratory suppression. In conclusion noxious gas-environment may influence potency of action, not release, of opioid. Less
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