Ciufo R, Nethery D, DiMarco A, Supinski G
Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Am J Respir Crit Care Med. 1995 Nov;152(5 Pt 1):1641-7. doi: 10.1164/ajrccm.152.5.7582308.
Some studies have suggested that protective mechanisms downregulate diaphragm activity during loaded breathing so as to prevent respiratory-muscle fatigue. Other work has indicated, however, that loading can sometimes elicit significant diaphragmatic fatigue, and that the development of fatigue may be related to alterations in diaphragmatic glutathione concentrations. One potential explanation for these discrepant observations is that the mechanism of respiratory failure may vary as a function of load magnitude, and that some loads evoke little fatigue whereas others produce substantial fatigue and glutathione alterations. The purpose of this study was to examine this issue by determining the diaphragmatic fatigue and alterations in glutathione concentrations produced by a range of inspiratory resistive loads. Experiments were performed on decerebrate rats divided into a control, unloaded group and a group loaded with small, medium, and large inspiratory resistive loads that were applied until respiratory failure occurred. After respiratory arrest, the animals' diaphragms were excised, an in vitro determination was done of diaphragm contractility characteristics, and samples of muscle were assayed for GSH (reduced glutathione) and GSSG (oxidized glutathione). We found that in vitro diaphragm force generation was severely reduced for loaded breathing, and surprisingly, that the magnitude of the low-frequency fatigue present was similar in the three loaded groups. Reductions in diaphragmatic GSH levels and increases in GSSG levels were found in all three loaded groups. Reductions in diaphragmatic GSH levels and increases in GSSG levels were found in all three loaded groups, but again, the magnitude of these changes were similar.(ABSTRACT TRUNCATED AT 250 WORDS)
一些研究表明，在负荷呼吸过程中，保护机制会下调膈肌活动，以防止呼吸肌疲劳。然而，其他研究表明，负荷有时会引发明显的膈肌疲劳，且疲劳的发展可能与膈肌谷胱甘肽浓度的变化有关。对于这些相互矛盾的观察结果，一种可能的解释是，呼吸衰竭的机制可能随负荷大小而变化，一些负荷引起的疲劳很小，而另一些则会导致严重的疲劳和谷胱甘肽变化。本研究的目的是通过确定一系列吸气阻力负荷所产生的膈肌疲劳和谷胱甘肽浓度变化来探讨这个问题。实验在去大脑大鼠身上进行，将其分为对照组（无负荷组）和分别施加小、中、大吸气阻力负荷直至呼吸衰竭的负荷组。呼吸停止后，切除动物的膈肌，对膈肌收缩特性进行体外测定，并对肌肉样本进行谷胱甘肽（还原型谷胱甘肽）和氧化型谷胱甘肽检测。我们发现，负荷呼吸时体外膈肌力量产生严重降低，而且令人惊讶的是，三个负荷组中低频疲劳的程度相似。在所有三个负荷组中均发现膈肌谷胱甘肽水平降低和氧化型谷胱甘肽水平升高。同样，所有三个负荷组中均发现膈肌谷胱甘肽水平降低和氧化型谷胱甘肽水平升高，但这些变化的程度相似。（摘要截选至250字）
