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红核在新生儿缺氧期间抑制呼吸。

Red nucleus inhibits breathing during hypoxia in neonates.

作者信息

Ackland G L, Noble R, Hanson M A

机构信息

Department of Obstetrics and Gynaecology, University College London, UK.

出版信息

Respir Physiol. 1997 Nov;110(2-3):251-60. doi: 10.1016/s0034-5687(97)00090-x.

Abstract

Conscious, anaesthetized and decerebrate young mammals respond to acute hypoxia with an initial increase in breathing followed by a fall to, or to below, pre-hypoxic levels--the biphasic ventilatory response. The ventilatory rise is due to sustained hypoxic stimulation of the peripheral chemoreceptors. We present evidence from brain stem and peripheral chemoreflex studies supporting the concept that, in addition to the peripheral chemoreceptors, hypoxia also activates brain stem pathways that inhibit ventilation. A key part of the inhibitory pathway is an area within the red nucleus. Destruction of this area in young decerebrate rabbits abolishes the ventilatory fall during hypoxia, yet has no effect on respiratory control during normoxia and does not affect arterial blood pressure changes in hypoxia. In support of this hypothesis, we report that there are neurones within the red nucleus that increase their discharge in hypoxia. The role of higher brain stem/hypothalamic function in central respiratory control during hypoxia in the fetus and neonate are considered.

摘要

清醒、麻醉和去大脑的幼年哺乳动物对急性缺氧的反应是,起初呼吸增加,随后降至或低于缺氧前水平——双相通气反应。通气增加是由于外周化学感受器受到持续的缺氧刺激。我们提供了来自脑干和外周化学反射研究的证据,支持这样一种观点,即除了外周化学感受器外,缺氧还激活抑制通气的脑干通路。抑制通路的一个关键部分是红核内的一个区域。破坏幼年去大脑兔的这个区域可消除缺氧时的通气下降,但对常氧时的呼吸控制没有影响,也不影响缺氧时的动脉血压变化。为支持这一假设,我们报告红核内有神经元在缺氧时放电增加。还考虑了胎儿和新生儿在缺氧时高级脑干/下丘脑功能在中枢呼吸控制中的作用。

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