Katzin D B, Rubinstein E H
Am J Physiol. 1976 Jul;231(1):179-84. doi: 10.1152/ajplegacy.1976.231.1.179.
Previous work suggests a primary vagal bradycardia during hypoxic excitation of the arterial chemoreceptors. In this study we examined whether tachycardia, resulting from withdrawal of vagal inhibition of the cardiac pacemaker, may also occur during hypoxia. Cats with cervical spinal section were ventilated with hypoxic gas mixtures or allowed to remain apneic in expiration while heart rate was continually monitored. During recovery from halothane anesthesia or following electrolytic midcollicular decerebration, the bradycardic response to hypoxic or asphyxic stimulation was reduced or was reversed to tachycardia. The extent of reduction or reversal of the bradycardia was positively correlated with the level of the arterial pressure which was adjusted by either hemorrhage or infusion of phenylephrine. These findings indicate a tachycardic component of the vagal response to hypoxia, integrated in the pontomedullary region of the brainstem and resulting from interaction between the chemoreceptor and baroreceptor reflexes.
先前的研究表明,在动脉化学感受器的低氧刺激过程中存在原发性迷走性心动过缓。在本研究中,我们检测了在低氧期间,由于迷走神经对心脏起搏器抑制作用的解除而导致的心动过速是否也会发生。对颈髓横断的猫用低氧混合气体进行通气,或使其在呼气时保持呼吸暂停,同时持续监测心率。在从氟烷麻醉恢复过程中或在电解中脑桥脑断离术后,对低氧或窒息刺激的心动过缓反应减弱或转为心动过速。心动过缓的降低或逆转程度与通过出血或输注去氧肾上腺素调节的动脉压水平呈正相关。这些发现表明,迷走神经对低氧的反应中存在心动过速成分,该成分整合于脑干的脑桥延髓区域,由化学感受器和压力感受器反射之间的相互作用所致。