Effects of prolonged mechanical ventilation and inactivity on piglet diaphragm function

Effects of prolonged mechanical ventilation and inactivity on piglet diaphragm function
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DOI:
10.1007/s00134-002-1207-8
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发表时间:
2002-03-01
影响因子:
38.9
通讯作者:
Eriksson, LI
Eriksson, LI
中科院分区:
医学1区
文献类型:
--
作者:
Radell, PJ;Remahl, S;Eriksson, LI

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目的:肌肉无力与制动、长时间机械通气、危重疾病和各种危重治疗有关。本研究采用模拟重症监护环境的动物模型,研究机械通气和静止5天对横隔膜收缩功能和神经生理功能的影响。设计:前瞻性实验室研究。单位:动物研究实验室。对象:2~3月龄仔猪7只,体重20~25公斤。干预:给予恒流、容量控制的机械通气(TV 12~15ml/kg,PEEP 3~5cmH(2)O,I:E 1:2),镇静不麻痹,防止自主呼吸。通过经静脉膈神经起搏实现诱发的膈肌收缩。测量方法和主要结果:使用跨膈压(PDI)测量来评估力频率关系。诱发的电生理指标包括最低刺激阈值和潜伏期,复合肌肉动作电位(CMAP)的波幅和时程,以及3 Hz重复刺激神经时的波幅。肺功能测量包括呼吸道压力、潮气量和微小容量,以及动态顺应性和阻力。在血流动力学、氧合和通气量方面没有明显的临床变化。肺容量的间接测量保持稳定。在所有测试频率下,PDI均下降了20%,同时诱发的CMAP波幅下降了30%(6.7+/-4.7 mV至4.5+/-3.9 mV,p=0.01),而CMAP阈值、潜伏期和持续时间在3 Hz重复刺激时未见明显降低。结论:在重症监护环境下延长机械通气时间的活体模型中,在镇静和完全不活动的情况下,5d的机械通气可导致膈肌收缩和激活障碍,而神经传导和神经肌肉传递不受影响。根据这些发现,所看到的变化很可能发生在外周肌肉水平。
Objectives: Muscle weakness is associated with immobilization, prolonged mechanical ventilation, critical illness and various critical care therapies. This study used an animal model simulating the critical care environment to investigate the effects of 5 days' mechanical ventilation and inactivity on diaphragm contractility and neurophysiologic function. Design: Prospective laboratory study. Setting: Animal research laboratory. Subjects: Seven 2-3 month old piglets weighing 20-25 kg. Interventions: The animals received constant-flow, volume-controlled mechanical ventilation (Tv 12-15 ml/kg, PEEP 3-5 cmH(2)O, I:E 1:2) and sedation without paralysis, and spontaneous breathing efforts were prevented. Evoked diaphragm contractions were achieved by transvenous phrenic nerve pacing. Measurements and main findings: Transdiaphragmatic pressure (Pdi) measurements were used to assess force frequency relationships. Evoked electrophysiologic measures included lowest stimulus threshold and latency, compound muscle action potential (CMAP) amplitude and duration, and amplitude during repetitive nerve stimulation at 3 Hz. Lung function measures included airway pressures, tidal and minute volumes, and dynamic compliance and resistance. There were no clinically significant changes in hemodynamics, oxygenation or ventilation. Indirect measures of lung volume remained stable. Pdi decreased by 20% at all frequencies tested and was accompanied by a 30% decrease in evoked CMAP amplitude, (6.7 +/- 4.7 mV to 4.5 +/- 3.9 mV, p=0.01) while CMAP threshold, latency and duration were unchanged and no significant decrement in amplitude was seen during repetitive stimulation at 3 Hz. Conclusion: In this in-vivo model of prolonged mechanical ventilation in an intensive caring setting, 5 days of mechanical ventilation with sedation and complete diaphragm inactivity resulted in disturbed diaphragm contractility and activation, while nerve conduction and neuromuscular transmission were not affected. Based on these findings, it is likely that the changes seen occur at the level of peripheral muscle.