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On the Cardioinhibitory Reflex Originating from the Superior Laryngeal Nerve

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On the Cardioinhibitory Reflex Originating from the Superior Laryngeal Nerve The Japanese Journal of Physiology 18,pp.453-461,1968 ON THE CARDIOINHIBITORY REFLEX ORIGINATING FROM THE SUPERIOR LARYNGEAL NERVE Juro IRIUCHIJIMAAND Mamoru KUMADA Institute for Medical Electronics and Department of Physiology, Faculty of Medicine,University of Tokyo Reflex inhibitory effects on the heart are not confined to the carotid sinus and depressor nerves.Almost all sensory nerves,when stimulated,can induce reflex inhibition of the heart beat under suitable conditions(MCDowALL,1956). The superior laryngeal nerve,containing afferent fibers from the mucous mem- brane of the upper larynx,is known to induce arrest or slowing of the heart relatively consistently(BRODIE and RUSSELL,1900;TOKITA, 964).Electrical stimulation of this nerve as well as chemical and mechanical stimulation of the laryngeal mucous membrane induces cardiac and respiratory arrest and blood pressure decrease.The recurrent laryngeal nerve produces no such effects.After bilateral vagotomy,electrical stimulation of the superior laryn- geal nerve induces cardiac acceleration and elevation of blood pressure(ToKITA, 1964).Since stimulation of the carotid sinus nerve usually induces cardiac deceleration and blood pressure decrease even after vagotomy,the above finding shows that the central mechanism of cardiovascular reflex originating from the superior laryngeal nerve is somewhat different from that of the sinus reflex.The present study was undertaken to examine the difference between the superior laryngeal and carotid sinus nerves in more detail by observing cardiac output and cardiac vagal discharge during the reflexes induced by stimulation of these nerves. METHODS Anesthesia.Mongrel dogs of either sex, weighing between 5 and 15kg,were given premedication of morphine hydrochloride(5mg/kg),injected subcutaneously,and an- esthetized one-half hour later with a mixture of alpha chloralose(40mg/kg)and ure- thane(300mg/kg),both dissolved in saline and injected intravenously.The saphenous vein was catheterized for additional injection of anesthetics. Hemodynamic and respiratory recordings.The trachea was cannulated for artificial ventilation with a positive pressure pump.The chest was opened in the left 4th inter- costal space and the pericardium was slit over the ascending aorta.A KOLIN type Received for publication September 9,1967 入 内 島十 郎, 熊 田 衛 453 454 J.IRIUCHIJIMA AND M.KUMADA coreless transducer(KoLIN,1959)was attached around the ascending aorta for the measurement of aortic flow .Then the chest wall was closed around the wires from the transducer.The pneumothorax was reduced ,whereupon the animal breathed normally. The flow signal recorded at the ascending aorta was integrated by a CR circuit with a time constant of 1 sec to obtain a measure of successive changes of cardiac output.Arterial blood pressure was recorded by connecting a cannulation of the femoral or carotid artery to a conventional strain-gauge electric manometer . The respiration of the animal was recorded with a thermistor(BT -15 ,NEC)placed in the tracheal cannula.During expiration , warm air passing by the thermistor dimin- ished its resistance and, during inspiration ,cold room air increased the resistance.The change of resistance of the thermistor with respiration was electrically recorded simul - taneously with blood pressure and cardiac output . Preparation of nerves.The superior laryngeal nerve and the carotid sinus nerve on either side were isolated and severed so that their central ends could be stimulated by a pair o silver-silver chloride electrodes .Rectangular currents isolated from earth were used for stimulation. For observation of action potentials in cardiac vagal fibers ,the right cervical vagus was freed from the surrounding tissues and cut in the midcervical region .A black plate was placed under the central cut end of the vagus,which was desheathed and split into fine strands with watchmaker's forceps under a binocular microscope .A trough formed by tying the edges of the skin wound to a metal ring fixed above the neck was filled with warmed paraffin ,so that the strands of the vagus were completely immrnersed for the prevention of drying .Action potentials from the nerve strands were recorded in the paraffin pool by mounting the strand on a pair of silver-silver chloride electrodes connected to a capacity coupled amplifier with a time constant of 2 msec .The action potentials were displayed on a cathode ray oscilloscope and photographed. In some animals,action potentials were recorded from the intrathoracic cardiac branch of the vagus.The thorax was opened by median sternotomy under positive pressure respiration.Cardiac branches of the right vagosympathetic trunk were sought under the superior caval vein,followed to beneath the auricle ,and cut as distally as possible.The right vagosympathetic trunk was cut at the level of the confluence of the azygos vein to the superior caval vein . All communication of the right vagus with the stellate ganglion and the sympathetic chain were cut and the right vagus with its cardiac branches was freed from the surrounding tissues up to the neck .The recurrent nerve was also severed at its origin from the vagus.The cardiac branches were then brought up to the neck and desheathed.Action potentials therefrom were recorded in a way similar to that for the strands of the cervical vagus. RESULTS Hemodyn,amic study.Arterial blood pressure(P)may be regarded as a monot- onically increasing function of the two variables,cardiac output(I)and peripheral resistance(R): ap aP P=f(I,R); >0, >0. (1) aI aR In total differential form, aP aP dP dI+ dR. (2) al aR LARYNGEAL NERVE REFLEX 455 When the curves of cardiac output and blood pressure are recorded simul- taneously as in FIG.1,the change in peripheral resistance can be estimated by comparing the two curves(IRIUCHIJIMA and OGATA,1964).A parallel change between cardiac output and blood pressure is observed when peripheral resistance is stationary.Under this condition,since the second term of the right hand side of equation(2)is O,a small increment of blood pressure(P) is proportional to that of cardiac output(I).Therefore,changes in peripheral resistance are detected by discrepancies between cardiac output and blood pressure.Thus,in case of the depressor reflex on sinus nerve stimulation (FIG.1,right panel),the initial part of blood pressure decrease was ascribable mainly to a decrease in cardiac output,because of the concomitant decrease of both cardiac output and blood pressure.However,in the latter part of the depressor reflex,a decrease in peripheral resistance was seen from the depres- sion of blood pressure(arrow,FIG.1)which was disproportionately large as compared with that of cardiac output. When the superior laryngeal nerve was stimulated,both cardiac output and blood pressure decreased as in FIG.1,left panel.In contrast to the de- SUP LARYNG N SINUS N 2V,I MSEC 50/SEC 2V,I MSEC,50/SEC FIG.1. Effect of stimulation of the superior laryngeal nerve(left panel) and the sinus nerve(right panel)on cardiac output,arterial blood pressure and respiration(from top downward,each panel).Blood pressure scale in mm Hg and,in respiratory recording,inspiration upward.Stimulation parameters were 5V,1 msec,and 50/sec for both nerves. pressor effect of the sinus nerve(right panel),cardiac output and blood pressure showed a parallel decrease on stimulation of the laryngeal nerve,indicating that the blood pressure decrease was ascribable solely to a decrease in cardiac output.Comparison of the effects of stimulation of the sinus and laryngeal nerves as in FIG.1 were performed in four dogs and the results were all consistent:a parallel decrease of cardiac output and blood pressure on laryngeal nerve stimulation and a disproportionately prolonged depression of blood pres- 456 J.IRIUCHIJIMA AND M.KUMADA sure curve on sinus nerve stimulation.In this series of experiments,stimu- lation parameters were 10-50 cps,1-5 msec,and 2-10V for both nerves.After strong stimulation of the laryngeal nerve a rise of blood pressure was observed when bradycardia had subsided.After bilateral vagotomy,as reported by TOKITA(1964),stimulation of the laryngeal nerve induced a pressor reflex instead of a depressor reflex.These findings indicate that the main cause of the depressor effect on stimulation of the laryngeal nerve is a decrease in cardiac output due to vagal bradycardia. In another series of experiments on three dogs,effects of stimulation of the sinus and laryngeal nerves on heart rate and blood pressure were studied without recording aortic flow.Since thoracotomy was unnecessary in this experiment,cardiovascular effects of both nerves could be compared under more natural conditions.The results were all consistent with those obtained in the above experiments in which cardiac output was measured:On laryngeal nerve stimulation,the decrease in blood pressure was always concomitant with bradycardia(FIG.2A).On stimulation of the sinus nerve,however,blood pressure recovered more slowly than the heart rate. Cardiac vagal discharge is periodically inhibited in the phase of inspiration by a direct inhibitory influence from the respiratory center on the cardiac A B FIG.2.Effect of tetanic stimulation of the superior laryngeal nerve (5V,1 msec,50/sec)on heart rate and blood pressure during spontaneous breathing(A)and during positive pressure artificial respiration(B). In both A and B,from top downward,heart rate,blood pressure and respiration(inspiration upward). LARYNGEAL NERVE REFLEX 457 vagal center(HEYMANS,1929;ANREP et al.,1935;KOEPCHEN et al.,1961; IRIUCHIJIMA and KUMADA,1964).On laryngeal nerve stimulation,since the respiratory center is inhibited(BRODIE and RUSSELL,1900),the cardiac vagal center is released from this periodical inhibition.The bradycardia on laryngeal nerve stimulation may be partly attributed to this secondary effect of respir- atory arrest.However,during artificial respiration when spontaneous respir- ation of the animal was suppressed,laryngeal nerve stimulation still induced bradycardia,though diminished in extent(FIG.2B).
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