Reflex cardiovascular depression during unilateral lung hyperinflation in the dog.
Reflex cardiovascular depression during unilateral lung hyperinflation in the dog.
复制标题
狗单侧肺过度充气期间反射性心血管抑制。
DOI：
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发表时间：
1979
影响因子：
15.9
通讯作者：
R. Johnson
中科院分区：
文献类型：
--
作者：
S. S. Cassidy;W. Eschenbacher;R. Johnson
我们检查了麻醉犬的肺过度膨胀是否反射性地降低了心输出量、每搏量、心率和血压，以及这些变化是否持续了一分钟以上。为消除肺过度充盈时对静脉回流和肺血流的机械限制，建立了一种开胸犬全肺动脉血流和全肺通气量均指向右肺，左侧颈迷走神经切断前后左肺过度充气的模型。在左肺充气至30 cm H(2)O的15分钟内，心率、每搏量和血压分别下降24%、20%和27%。心率在1分钟内增加到充气前水平，但每搏输出量和血压在肺充气至少15分钟时保持低迷状态。通气后，每搏出血量和血压在1分钟内恢复到对照水平。左侧迷走神经干在颈部的分离中断了左肺的所有自主神经传入和传出神经，但保留了心脏的右侧迷走神经交感和副交感传入神经和传出神经。左颈迷走神经切断术后，左肺过度充气时心率、每搏量和血压的一过性下降大大减少或消除。这些结果表明，单侧肺过度膨胀反射性地降低了心率和血压，而心率和血压随着时间的推移得到了部分补偿，并反射性地抑制了每搏量，这种情况一直没有补偿，直到肺收缩。这些发现可能解释了在局部肺过度扩张时观察到的心血管功能抑制，特别是在正压通气时。
We have examined whether lung hyperinflation in the anesthetized dog reflexly depresses cardiac output, stroke volume, heart rate, and blood pressure and whether these changes persist for more than a minute. To eliminate any mechanical restriction to venous return and pulmonary blood flow during lung hyperinflation, a model was developed in which all pulmonary artery blood flow and all ventilation were directed to the right lung in dogs with widely open chest and the left lung was hyperinflated before and after left cervical vagotomy. Heart rate, stroke volume, and blood pressure decreased by 24, 20, and 27%, respectively, within 15 s of left lung inflation to 30 cm H(2)O. Heart rate increased to preinflation levels by 1 min, but stroke volume and blood pressure remained depressed during lung hyperinflation for at least 15 min. Upon deflation, stroke volume and blood pressure returned to control levels within 1 min. Division of the left vagosympathetic trunk at the neck interrupted all autonomic afferent and efferent nerves of the left lung, but left intact the right vagal sympathetic and parasympathetic afferent and efferent nerves of the heart. After left cervical vagotomy the transient fall in heart rate, stroke volume, and blood pressure during left lung hyperinflation was greatly reduced or eliminated. These results suggest that unilateral lung hyperinflation reflexly depresses heart rate and blood pressure, which are partially compensated with time, and reflexly depresses stroke volume, which persists uncompensated until the lung is deflated. These findings may explain the depressed cardiovascular function observed during regional lung overdistention especially when it occurs during positive pressure ventilation.