Adverse effects of myasthenia gravis on rat phrenic diaphragm contractile performance.
Adverse effects of myasthenia gravis on rat phrenic diaphragm contractile performance.
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重症肌无力对大鼠膈肌收缩性能的不利影响。
DOI：
10.1152/japplphysiol.01266.2003
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Kaminski,HenryJ
中科院分区：
文献类型：
--
作者：
vanLunteren,Erik;Moyer,Michelle;Kaminski,HenryJ
重症肌无力对呼吸系统有不同的影响，从没有异常到危及生命的呼吸衰竭。大鼠自身免疫性重症肌无力中膈肌收缩性能的研究。大鼠接受单克隆抗体，识别乙酰胆碱受体决定簇（或非活性抗体）; 3天后，膈神经和膈肌进行了体外研究。肌无力大鼠分为两组，当在完整动物中测试时，具有正常与受损肢体肌肉功能的那些（“轻度”和“重度”肌无力）。与对照动物相比，重度（P< 0.01）和轻度（P< 0.05）肌无力的基线膈肌抽动力均降低（抽动力：正常1，352 ± 140，轻度肌无力672 ± 99，重度肌无力687 ± 74 g/cm 2）。然而，只有严重的肌无力膈肌有受损的膈肌耐力，基于显着刺激初期峰值力下降速度加快（P< 0.05）（正常、轻度肌无力和重度肌无力分别为0.02 ± 0.02、0.03 ± 0.01和0.09 ± 0.01%/脉冲，连续刺激时）和肌内疲劳（重度肌无力组肌内肌力下降达30.5 ± 7.4%，而正常和轻度肌无力组无，P< 0.01）。与连续刺激相比，间歇刺激对重症肌无力膈肌的肌力有保护作用（间歇刺激2,000次后肌力为初始值的31.4 ± 2.0%，连续刺激2,000次后肌力为初始值的13.0 ± 2.1%，P< 0.01），但对正常膈肌无保护作用。这些数据表明，基线力和疲劳可能会受到不同程度的重症肌无力的严重程度，并进一步提供了一种机制，呼吸模式的改变可能会恶化神经肌肉疾病的呼吸肌功能。
Myasthenia gravis has variable effects on the respiratory system, ranging from no abnormalities to life-threatening respiratory failure. Studies characterized diaphragm muscle contractile performance in rat autoimmune myasthenia gravis. Rats received monoclonal antibody that recognizes acetylcholine receptor determinants (or inactive antibody); 3 days later, phrenic nerve and diaphragm were studied in vitro. Myasthenic rats segregated into two groups, those with normal vs. impaired limb muscle function when tested in intact animals (“mild” and “severe” myasthenic). Baseline diaphragm twitch force was reduced for both severe (P< 0.01) and mild (P< 0.05) myasthenic compared with control animals (twitch force: normal 1,352 ± 140, mild myasthenic 672 ± 99, severe myasthenic 687 ± 74 g/cm2). However, only severe myasthenic diaphragm had impaired diaphragm endurance, based on significantly (P< 0.05) accelerated rate of peak force decline during the initial period of stimulation (0.02 + 0.02, 0.03 ± 0.01, and 0.09 ± 0.01%/pulse for normal, mild myasthenic, and severe myasthenic, respectively, during continuous stimulation) and intratrain fatigue (up to 30.5 ± 7.4% intratrain force drop in severe myasthenic vs. none in normal and mild myasthenic,P< 0.01). Furthermore, compared with continuous stimulation, intermittent stimulation had a protective effect on force of severe myasthenic diaphragm (force after 2,000 pulses was 31.4 ± 2.0% of initial during intermittent stimulation vs. 13.0 ± 2.1% of initial during continuous stimulation,P< 0.01) but not on normal diaphragm. These data indicate that baseline force and fatigue may be affected to different extents by varying severity of myasthenia gravis and furthermore provide a mechanism by which alterations in breathing pattern may worsen respiratory muscle function in neuromuscular diseases.
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