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纳洛酮会改变对吸气性气流阻力负荷的早期反应。

Naloxone alters the early response to an inspiratory flow-resistive load.

作者信息

Scardella A T, Santiago T V, Edelman N H

机构信息

Department of Medicine, University of Medicine and Dentistry, New Jersey-Robert Wood Johnson Medical School, New Brunswick 08903-0019.

出版信息

J Appl Physiol (1985). 1989 Nov;67(5):1747-53. doi: 10.1152/jappl.1989.67.5.1747.

DOI:10.1152/jappl.1989.67.5.1747
PMID:2532192
Abstract

In a previous study in unanesthetized goats, we demonstrated that cerebrospinal fluid levels of beta-endorphin were significantly elevated after 2.5 h of inspiratory flow-resistive loading. Naloxone (NLX) (0.1 mg/kg) administration partially and transiently reversed the tidal volume depression seen during loading. In the current study, we tested the hypothesis that endogenous opioid elaboration results in depression of respiratory output to the diaphragm. In six studies of five unanesthetized goats, tidal volume (VT), transdiaphragmatic pressure (Pdi), diaphragmatic electromyogram (EMGdi), and arterial blood gases were monitored. A continuous NLX (0.1 mg/kg) or saline (SAL) infusion was begun 5 min before an inspiratory flow-resistive load of 120 cmH2O.l-1.s was imposed. Our data show that the depression of VT induced by the load was prevented by NLX as early as 15 min and persisted for 2 h. At 2 h, Pdi was still 294 +/- 45% of the base-line value compared with 217 +/- 35% during SAL. There was no difference in EMGdi between the groups at any time. However, the augmentation of Pdi was associated with a greater increase in end-expiratory gastric pressure in the NLX group. We conclude that the reduction in VT and Pdi associated with endogenous opioid elaboration is not mediated by a decrease in neural output to the diaphragm, but it appears to be the result of a decrease in respiratory output to the abdominal muscles.

摘要

在之前一项针对未麻醉山羊的研究中,我们证实,在进行2.5小时吸气性气流阻力负荷后,脑脊液中β-内啡肽水平显著升高。给予纳洛酮(NLX)(0.1毫克/千克)可部分且短暂地逆转负荷期间出现的潮气量降低。在本研究中,我们检验了内源性阿片类物质的释放导致膈神经输出减少这一假说。在对5只未麻醉山羊进行的6项研究中,监测了潮气量(VT)、跨膈压(Pdi)、膈肌肌电图(EMGdi)和动脉血气。在施加120厘米水柱·升-1·秒的吸气性气流阻力负荷前5分钟,开始持续输注NLX(0.1毫克/千克)或生理盐水(SAL)。我们的数据表明,早在15分钟时,NLX就可预防负荷诱导的VT降低,且这种作用持续2小时。2小时时,Pdi仍为基线值的294±45%,而在输注SAL期间为217±35%。两组在任何时间的EMGdi均无差异。然而,NLX组Pdi的增加与呼气末胃内压的更大升高有关。我们得出结论,与内源性阿片类物质释放相关的VT和Pdi降低并非由膈神经输出减少介导,而似乎是呼吸对腹部肌肉输出减少的结果。

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