Department of Comparative Biosciences, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706-1102, USA.
Respir Physiol Neurobiol. 2011 Mar 15;175(3):303-9. doi: 10.1016/j.resp.2010.12.005. Epub 2010 Dec 15.
We hypothesized that reduced respiratory neural activity elicits compensatory mechanisms of plasticity that enhance respiratory motor output. In urethane-anesthetized and ventilated rats, we reversibly reduced respiratory neural activity for 25-30 min using: hypocapnia (end tidal CO(2)=30 mmHg), isoflurane (~1%) or high frequency ventilation (HFV; ~100 breaths/min). In all cases, increased phrenic burst amplitude was observed following restoration of respiratory neural activity (hypocapnia: 92±22%; isoflurane: 65±22%; HFV: 54±13% baseline), which was significantly greater than time controls receiving the same surgery, but no interruptions in respiratory neural activity (3±5% baseline, p<0.05). Hypocapnia also elicited transient increases in respiratory burst frequency (9±2 versus 1±1bursts/min, p<0.05). Our results suggest that reduced respiratory neural activity elicits a unique form of plasticity in respiratory motor control which we refer to as inactivity-induced phrenic motor facilitation (iPMF). iPMF may prevent catastrophic decreases in respiratory motor output during ventilatory control disorders associated with abnormal respiratory activity.
我们假设呼吸神经活动的减少会引发代偿性的可塑性机制,从而增强呼吸运动输出。在使用乌拉坦麻醉和通气的大鼠中,我们使用以下方法可逆地减少呼吸神经活动 25-30 分钟:低碳酸血症(呼气末二氧化碳=30mmHg)、异氟烷(1%)或高频通气(HFV;100 次/分钟)。在所有情况下,恢复呼吸神经活动后观察到膈神经爆发幅度增加(低碳酸血症:92±22%;异氟烷:65±22%;HFV:54±13%基线),明显大于接受相同手术但呼吸神经活动无中断的时间对照(3±5%基线,p<0.05)。低碳酸血症还引起呼吸爆发频率的短暂增加(9±2 次/分钟比 1±1 次/分钟,p<0.05)。我们的结果表明,呼吸神经活动的减少会引发呼吸运动控制中的一种独特形式的可塑性,我们称之为不活动诱导的膈神经运动易化(iPMF)。iPMF 可能会防止与异常呼吸活动相关的通气控制障碍期间呼吸运动输出的灾难性下降。