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首页> 外文期刊>American Journal of Physiology >A mapping study of cardiorespiratory responses to chemical stimulation of the midline medulla oblongata in ventilated and freely breathing rats.
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A mapping study of cardiorespiratory responses to chemical stimulation of the midline medulla oblongata in ventilated and freely breathing rats.

机译：对通气和自由呼吸大鼠中线延髓化学刺激的心肺反应的作图研究。

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The aim of this study was to examine the cardiorespiratory effects of chemically stimulating neurons in the midline medulla oblongata (MM) of artificially ventilated and freely breathing anesthetized rats. Earlier studies reported that stimulation of the MM elicits increases or decreases in mean arterial pressure (MAP) and phrenic nerve activity, depending on the mode and site of stimulation, anesthetic, and species. In the first series of experiments, rats were anesthetized with urethane, artificially ventilated, paralyzed, and bilaterally vagotomized. The rostrocaudal extent of the MM was mapped by microinjections of DL-homocysteic acid or L-glutamate (both 100 mM, 100 nl), and, in line with previous studies, most injections produced only small responses in MAP, heart rate, and splanchnic sympathetic nerve activity. Increases in respiratory parameters were evoked in caudal regions. However, activation of a discrete region of the MM at the level of the caudal pole of the facial nucleus (CP7) consistently caused a dramatic reduction in phrenic nerve amplitude and/or frequency and, in six rats, produced a prolonged apnea. The second series of experiments was carried out on freely breathing pentobarbitone sodium-anesthetized rats, with a diaphragmatic electromyogram used to monitor respiratory activity. Respiratory activity could again be abolished at CP7 after microinjections of glutamate (100 mM, 50 nl); however, these responses were accompanied by large decreases in MAP and moderate reductions in heart rate. This depression of respiratory activity may be due to activation of propriobulbar inhibitory neurons that project to known respiratory centers in the brain stem.
机译：这项研究的目的是检查人工通风和自由呼吸的麻醉大鼠中线延髓（MM）中化学刺激神经元的心肺功能。较早的研究报道，对MM的刺激会引起平均动脉压（MAP）和activity神经活动的增加或减少，具体取决于刺激的方式和部位，麻醉剂和种类。在第一个系列实验中，大鼠用氨基甲酸乙酯麻醉，人工通气，瘫痪，双侧迷路。通过微量注射DL-同型半胱氨酸或L-谷氨酸（均为100 mM，100 nl）绘制MM的后尾巴范围，并且与以前的研究一致，大多数注射仅在MAP，心率和内脏方面产生很小的反应交感神经活动。引起尾端呼吸参数增加。然而，在面核尾极水平（CP7）处MM离散区域的激活始终导致神经振幅和/或频率急剧降低，并且在六只大鼠中产生了长时间的呼吸暂停。第二组实验是在自由呼吸的戊巴比妥钠麻醉的大鼠上进行的，其中a肌肌电图用于监测呼吸活动。微量注射谷氨酸（100 mM，50 nl）后，CP7的呼吸活性可能会再次消失。然而，这些反应伴随着MAP的大幅降低和心率的适度降低。这种呼吸活动的降低可能是由于投射到脑干中已知的呼吸中枢的球突抑制神经元的激活所致。

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