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纳洛酮对吸气负荷期间膈肌肌电图频谱变化的影响。

Effect of naloxone on spectral shifts of the diaphragm EMG during inspiratory loading.

作者信息

Petrozzino J J, Scardella A T, Li J K, Krawciw N, Edelman N H, Santiago T V

机构信息

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

出版信息

J Appl Physiol (1985). 1990 Apr;68(4):1376-85. doi: 10.1152/jappl.1990.68.4.1376.

Abstract

Shifts in the power spectrum of the diaphragm EMG to lower frequencies may occur in the presence of fatiguing inspiratory flow-resistive loads (IRL). However, such a shift of the centroid frequency (fc) could follow a reduction in central output through a differential reduction in end-inspiratory high-frequency power (HFP). In unanesthetized goats, we tested the hypothesis that activation of the endogenous opioid system by IRL would differentially reduce central respiratory output, causing a reduction in fc. IRL was imposed for 180 min after which naloxone (0.1 mg/kg, NLX) was given. fc was computed from the power spectral density estimated by the Welch method. IRL reduced fc from 148.0 +/- 9.8 (SE) Hz at base line to 141.1 +/- 8.9 Hz or to 95.5 +/- 1.3% of base line by 180 min (both P less than 0.05). NLX increased fc to 148.9 +/- 9.9 Hz or to 100.6 +/- 1.1% of base line (both P less than 0.05). The decline in fc during IRL was found to be the result of a reduction in HFP, predominantly toward the end of inspiration. The reversibility of this fc shift with NLX suggests a central mechanism consequent to elaboration of endogenous opioids and not a peripheral (muscular) event consequent to muscle fatigue.

摘要

在存在导致疲劳的吸气性气流阻力负荷(IRL)的情况下,膈肌肌电图的功率谱可能会向低频偏移。然而,这种质心频率(fc)的偏移可能是由于吸气末高频功率(HFP)的差异减少导致中枢输出降低所致。在未麻醉的山羊中,我们检验了以下假设:IRL激活内源性阿片系统会差异性地降低中枢呼吸输出,导致fc降低。施加IRL 180分钟后给予纳洛酮(0.1 mg/kg,NLX)。fc通过韦尔奇方法估计的功率谱密度计算得出。IRL使fc从基线时的148.0±9.8(SE)Hz降至141.1±8.9 Hz,或在180分钟时降至基线的95.5±1.3%(两者P均小于0.05)。NLX使fc增加至148.9±9.9 Hz,或增至基线的100.6±1.1%(两者P均小于0.05)。发现IRL期间fc的下降是HFP降低的结果,主要发生在吸气末期。fc偏移被NLX逆转表明这是内源性阿片释放后的一种中枢机制,而非肌肉疲劳后的外周(肌肉)事件。

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