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向麻醉兔左心室内注入枸椽酸钠,首先引起振幅增高、频率加快的呼吸兴奋相,切断两侧主动脉弓减压神经后此效应依然存在,阿托平前处理并切断两侧颈迷走神经后此效应依然存在;切断两侧窦神经后呼吸兴奋相不再呈现,选择性破坏颈动脉体化学感受器而同时保留压力感受器也使呼吸兴奋相不再呈现。上述结果说明,家兔心内注射枸橼酸钠引起呼吸兴奋的传入纤维行走于窦神经而非行走于减压神经或迷走神经之中,此效应的感受器是颈动脉体化学感受器。向右侧椎动脉内注入枸橼酸钠1.6～60.0mg/kg,均引起呼吸兴奋。心内注射枸橼酸钠引起动物呼吸减慢以至完全停止时颈部隔神经的节律性放电亦逐渐减慢以至完全停止,而同时直接刺激膈神经外周端仍能引起膈肌收缩,说明此种呼吸抑制是呼吸中枢节律性放电活动停止所致并非由于神经肌接头或呼吸肌麻痹;呼吸中枢的节律性放电抑制不是来自枸橼酸钠对中枢神经系统的直按作用,可能是由于低血压导致脑部血供不足所致。
Into the anesthetized rabbit left ventricular injection of sodium citrate, first caused by the amplitude increased, the frequency of the respiratory excited phase, cut off both sides of the aortic arch decompression after this effect still exists, atropine before and after treatment of both cervical vagus nerve The effect still exists; cut off both sides of the sinus nerve respiratory excitability is no longer present, selective destruction of carotid body chemoreceptors while retaining the baroreceptor excite the respiratory phase is no longer present. The above results show that intracardiac injection of sodium citrate in rabbits induces the excitement of the afferent fibers to walk in the sinus rather than walking in the decompression or vagus nerve. The receptors for this effect are carotid body chemoreceptors. Into the right vertebral artery sodium citrate 1.6 ~ 60.0mg / kg, are caused by respiratory excitement. Intracardiac injection of sodium citrate caused animal breathing slowed down and even stop completely when the rhythmic discharge of the cervical septal nerve also gradually slowed down and even stopped, while direct stimulation of the peripheral edge of the phrenic nerve can still cause diaphragmatic contraction, indicating that such breathing Inhibition is due to respiratory rhythmic arrhythmic discharge stopped due to neuromuscular junction or respiratory muscle paralysis; rhythmic discharge inhibition of the respiratory center is not from sodium citrate on the central nervous system, direct press, may be due to hypotension leads to brain Department of blood supply due to inadequate.