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呼吸调整中枢切除术后对高碳酸血症和低氧血症的不同反应。

Differing responses to hypercapnia and hypoxia following pneumotaxic center ablation.

作者信息

Saint John W M

出版信息

Respir Physiol. 1975 Jan;23(1):1-9. doi: 10.1016/0034-5687(75)90066-3.

Abstract

The respiratory responses of 21 cats were examined upon exposure to hypercapnia and isocapnic hypoxia. Animals having bilateral electrolytic lesions localized in the pontile pneumotaxic center exhibited hypercapnia-induced minute volumes which were significantly less than those of unlesioned control cats. The hypoxia-induced minute volumes of pneumotaxic lesioned animals, examined at isocapnic alveolar gas partial pressures, were likewise significantly less than control animals at end-expired oxygen partial pressures (PAO2) in excess of 65.0 mm Hg. At PAO2 levels below 65.0 mmHg. the minute volume of experimental animals rose sharply and became statistically indistinguishable from that of the unlesioned cats. The placement of control brain stem lesions typically produced no significant alterations in the respiratory responses to hypoxia or hypercapnia. It was concluded that the pneumotaxic center constitutes an integral component of the central chemoreceptor CO1-H+ CONTROLLING SUBSYSTEM. The concept of differing anatomical sites within the brain stem serving integrative functions for central chemoreceptor and peripheral chemoreceptor afferent stimuli is also supported.

摘要

对21只猫在暴露于高碳酸血症和等碳酸性低氧环境时的呼吸反应进行了检查。双侧电解损伤位于脑桥呼吸调整中枢的动物,其高碳酸血症诱导的每分通气量显著低于未损伤的对照猫。在等碳酸性肺泡气分压条件下检查,呼吸调整中枢损伤动物的低氧诱导每分通气量,在呼气末氧分压(PAO2)超过65.0 mmHg时,同样显著低于对照动物。在PAO2水平低于65.0 mmHg时,实验动物的每分通气量急剧上升,在统计学上与未损伤猫的每分通气量没有差异。对照脑干损伤的定位通常不会对低氧或高碳酸血症的呼吸反应产生显著改变。得出的结论是,呼吸调整中枢是中枢化学感受器CO2-H+控制子系统的一个组成部分。脑干内不同解剖部位为中枢化学感受器和外周化学感受器传入刺激发挥整合功能的概念也得到了支持。

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