Elsner R, Angell-James J E, de Burgh Daly M
Am J Physiol. 1977 May;232(5):H517-25. doi: 10.1152/ajpheart.1977.232.5.H517.
In the anesthetized spontaneously breathing harbor seal Phoca vitulina stimulation of the carotid body chemoreceptors by intracarotid injections of sodium cyanide or by hypoxic hypercapnic blood causes an increase in tidal volume, respiratory frequency, and respiratory minute volume. The heart rate invariably decreased. Experimental dives caused apnea and bradycardia. When the carotid bodies are stimulated within 10 s of the commencement of a dive, the chemoreceptor-respiratory response is abolished, but the chemoreceptor-cardioinhibitory response is considerably enhanced. Electrical stimulation of the central cut end of a superior laryngeal nerve also causes apnea and bradycardia; stimulation of the carotid body now fails to produce a respiratory response but the cardioinhibitory effect is enhanced. These results indicate that the carotid bodies cause reflexly hyperventilation and bradycardia, and that these responses are considerably modified by other inputs to the central nervous system.
在麻醉状态下自主呼吸的斑海豹(Phoca vitulina)中,通过颈内注射氰化钠或输入低氧高碳酸血症血液刺激颈动脉体化学感受器,会导致潮气量、呼吸频率和每分钟呼吸量增加。心率则始终下降。实验性潜水会导致呼吸暂停和心动过缓。在潜水开始后10秒内刺激颈动脉体,化学感受器 - 呼吸反应会被消除,但化学感受器 - 心脏抑制反应会显著增强。电刺激喉上神经的中枢切断端也会导致呼吸暂停和心动过缓;此时刺激颈动脉体无法产生呼吸反应,但心脏抑制作用会增强。这些结果表明,颈动脉体会引起反射性过度通气和心动过缓,并且这些反应会被中枢神经系统的其他输入信号显著改变。