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清醒犬对渐进性高碳酸血症的反应中呼吸性窦性心律不齐的增强。

Augmentation of respiratory sinus arrhythmia in response to progressive hypercapnia in conscious dogs.

作者信息

Yasuma F, Hayano J

机构信息

First Department of Internal Medicine, Nagoya University School of Medicine, Nagoya 466-8550, Japan.

出版信息

Am J Physiol Heart Circ Physiol. 2001 May;280(5):H2336-41. doi: 10.1152/ajpheart.2001.280.5.H2336.

Abstract

Respiratory sinus arrhythmia (RSA) may serve to enhance pulmonary gas exchange efficiency by matching pulmonary blood flow with lung volume within each respiratory cycle. We examined the hypothesis that RSA is augmented as an active physiological response to hypercapnia. We measured electrocardiograms and arterial blood pressure during progressive hypercapnia in conscious dogs that were prepared with a permanent tracheostomy and an implanted blood pressure telemetry unit. The intensity of RSA was assessed continuously as the amplitude of respiratory fluctuation of heart rate using complex demodulation. In a total of 39 runs of hypercapnia in 3 dogs, RSA increased by 38 and 43% of the control level when minute ventilation reached 10 and 15 l/min, respectively (P < 0.0001 for both), and heart rate and mean arterial pressure showed no significant change. The increases in RSA were significant even after adjustment for the effects of increased tidal volume, respiratory rate, and respiratory fluctuation of arterial blood pressure (P < 0.001). These observations indicate that increased RSA during hypercapnia is not the consequence of altered autonomic balance or respiratory patterns and support the hypothesis that RSA is augmented as an active physiological response to hypercapnia.

摘要

呼吸性窦性心律不齐(RSA)可能通过在每个呼吸周期内使肺血流量与肺容量相匹配来提高肺气体交换效率。我们检验了这样一种假设,即RSA作为对高碳酸血症的一种主动生理反应而增强。我们在对有意识的犬进行渐进性高碳酸血症期间测量了心电图和动脉血压,这些犬已进行了永久性气管切开术并植入了血压遥测装置。使用复解调法将RSA的强度作为心率呼吸波动的幅度进行连续评估。在3只犬总共39次高碳酸血症实验中,当分钟通气量分别达到10和15升/分钟时,RSA分别比对照水平增加了38%和43%(两者P均<0.0001),心率和平均动脉压无显著变化。即使在对潮气量增加、呼吸频率和动脉血压呼吸波动的影响进行校正后,RSA的增加仍具有显著性(P<0.001)。这些观察结果表明,高碳酸血症期间RSA的增加不是自主神经平衡或呼吸模式改变的结果,并支持RSA作为对高碳酸血症的一种主动生理反应而增强的假设。

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