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刺激左心房感受器对心脏的反射效应。

Reflex effects on the heart of stimulating left atrial receptors.

作者信息

Furnival C M, Linden R J, Snow H M

出版信息

J Physiol. 1971 Oct;218(2):447-63. doi: 10.1113/jphysiol.1971.sp009627.

Abstract
  1. Stimulation of left atrial receptors, by distension of the pulmonary vein/left atrial junctions, is known to cause a reflex increase in heart rate; the efferent pathway is known to be solely in the sympathetic nerves.2. In expectation of a concomitant positive inotropic response the effect of stimulating the left atrial receptors on the inotropic state of the left ventricle was studied, using as a known sensitive index of inotropic changes the maximal rate of rise of pressure in the left ventricle (dP/dt max).3. Stimulation of left atrial receptors resulted in an increase in heart rate but there were no significant concomitant changes in dP/dt max.4. It is concluded that activity in this discrete efferent pathway does not include an inotropic effect on the left ventricle and therefore the reflex involves only those sympathetic nerves which innervate the sinu-atrial node.5. The possible function of atrial receptors in the regulation of heart volumes is discussed.
摘要
  1. 通过扩张肺静脉/左心房连接处来刺激左心房受体,已知会引起心率反射性增加;传出通路已知仅存在于交感神经中。

  2. 预期会有伴随的正性肌力反应,于是使用左心室压力最大上升速率(dP/dt max)作为已知的敏感的肌力变化指标,研究了刺激左心房受体对左心室肌力状态的影响。

  3. 刺激左心房受体导致心率增加,但dP/dt max没有显著的伴随变化。

  4. 得出的结论是,这条离散的传出通路的活动不包括对左心室的正性肌力作用,因此该反射仅涉及那些支配窦房结的交感神经。

  5. 讨论了心房受体在调节心脏容量方面的可能功能。

相似文献

2
Atrial receptors and heart rate: the efferent pathway.心房感受器与心率:传出通路
J Physiol. 1975 Aug;249(3):581-90. doi: 10.1113/jphysiol.1975.sp011031.
3
The effects of distension of the pulmonary vein-atrial junctions upon peripheral vascular resistance.
J Physiol. 1970 Mar;207(1):1-14. doi: 10.1113/jphysiol.1970.sp009044.
4
Gradation of the reflex response from atrial receptors.心房感受器反射反应的分级
J Physiol. 1975 Oct;251(2):561-7. doi: 10.1113/jphysiol.1975.sp011108.

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2
The central and reflex regulation of the heart rate.心率的中枢调节与反射调节
J Physiol. 1926 Apr 23;61(2):215-31. doi: 10.1113/jphysiol.1926.sp002284.

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