Neuroinhibition in the regulation of emesis

Elucidation of an inhibitory system in the regulation of emesis is presented in this report. Emesis preceded by retching, can be induced in the dog by appropriate electrical stimulation of abdominal vagus nerves at the supradiaphragmatic level. Failure to produce retching or emesis by electrical stimulation of the cervical vagus trunk suggests either that the abdominal vagal emetic afferent does not course in the cervical vagus or that fibers inhibitory to emesis are present. This report presents evidence for afferent fibers inhibitory to retching and emesis in the cervical vagus. Retching and emesis resulting from stimulation of the supradiaphragmatic vagus can be prevented by either transection of the cervical vagus or simultaneous stimulation of the cervical vagus trunk. In addition, retching and emesis occur with stimulation of a fine nerve bundle dissected from the cervical vagus trunk. That the afferent pathway inhibitory to retching and emesis involves pulmonary afferents is suggested by the observation that hyperventilation occurs with stimulation of the cervical vagus trunk.Research supported by U.S.P.H.S. Grant No. FR05339-07     

Effect of practolol on experimental hypertension in dogs]

In the dog, the intra-venous injection of practolol (1 to 3 mg/kg) reduces the hypertension provoked by vagotomy and sino-aortic nerves section, or by intra-venous administration of potassium cyanide. But practolol differs from propranolol ; he does not modify hypertension observed after electrical stimulation of central end of saphene, laryngeal superior, or vagus nerf.     

Laryngeal motor control in frogs: Role of vagal and laryngeal feedback

Using decerebrate frogs (Rana catesbeiana), we investigated the role of vagal and laryngeal sensory feedback in controlling motor activation of the larynx. Vagal and laryngeal nerve afferents were activated by electrical stimulation of the intact vagal and laryngeal nerves. Pulmonary afferents were activated by lung inflation. Reflex responses were recorded by measuring efferent activity in the laryngeal branch of the vagus (Xℓ) and changes in glottal aperture. Two glottic closure reflexes were identified, one evoked by lung inflation or electrical stimulation of the main branch of the vagus (Xm), and the other by electrical stimulation of Xℓ. Lung inflation evoked a decrementing burst of Xℓ efferent activity and electrical stimulation of Xm resulted in a brief burst of Xℓ action potentials. Electrical stimulation of Xℓ evoked a triphasic mechanical response, an abrupt glottal constriction followed by glottal dilatation followed by a long-lasting glottal constriction. The first phase was inferred to be a direct (nonreflex) response to the stimulus, whereas the second and third represent reflex responses to the activation of laryngeal afferents. Intracellular recordings of membrane potential of vagal motoneurons of lung and nonlung types revealed EPSPs in both types of neurons evoked by stimulation of Xm or Xℓ, indicating activation of glottal dilator and constrictor motoneurons. In summary, we have identified two novel reflexes producing glottic closure, one stimulated by activation of pulmonary receptors and the other by laryngeal receptors. The former may be part of an inspiratory terminating reflex and the latter may represent an airway protective reflex. © 1997 John Wiley & Sons, Inc. J Neurobiol 33: 213–222, 1997     

Functional anatomy of the vagal innervation of the cervical trachea of the dog.

The canine cervical trachea has been used for numerous studies regarding the neural control of tracheal smooth muscle. The purpose of the present study was to determine whether there is lateral dominance by either the left or right vagal innervation of the canine cervical trachea. In anesthetized dogs, pressure in the cuff of the endotracheal tube was used as an index of smooth muscle tone in the trachea. After establishment of tracheal tone, as indicated by increased cuff pressure, either the right or left vagus nerve was sectioned followed by section of the contralateral vagus. Sectioning the right vagus first resulted in total loss of tone in the cervical trachea, whereas sectioning the left vagus first produced either a partial or no decrease in tracheal tone. After bilateral section of the vagi, cuff pressure was recorded during electrical stimulation of the rostral end of the right or left vagus. At the maximum current strength used, stimulation of the left vagus produced tracheal constriction that averaged 28.5% of the response to stimulation of the right vagus (9.0 +/- 1.8 and 31.6 +/- 2.5 mmHg, respectively). In conclusion, the musculature of cervical trachea in the dog appears to be predominantly controlled by vagal efferents in the right vagus nerve.     

Vagal innervation of guinea pig bronchial smooth muscle

We isolated the guinea pig right bronchus with the vagus nerves intact and evaluated the changes in isometric tension of the smooth muscle in response to nerve stimulation. Brief (10-s) trains of electrical field stimulation or vagus nerve stimulation caused a biphasic contraction: the "first phase" sensitive to atropine and the "second phase" sensitive to capsaicin. The two phases could be dissociated by adjusting the stimulus intensity; greater stimulus intensities (pulse durations or voltage) were required to evoke the capsaicin-sensitive phase. When stimulated at 30-min intervals, the magnitude of both phases of the contractions declined over a 2-h period of repeated stimulation; however, this was prevented by indomethacin. Stimulation of the left vagus nerve resulted in a monophasic contraction of the right bronchus, with little evidence of a capsaicin-sensitive phase. Blocking neurotransmission through the bronchial ganglion, as monitored by intracellular recording techniques, abolished the first-phase contraction but had no effect on the capsaicin-sensitive phase. Selective blockade of muscarinic M1 receptors had no effect on vagus nerve-mediated contractions. The results demonstrate that the left and right vagus nerves carry preganglionic fibers to the right bronchial ganglion. The right but not the left vagus nerve also carries capsaicin-sensitive afferent fibers that, when stimulated, result in a persistent contraction of the right bronchus. Finally, we provide functional and electrophysiological evidence supporting the hypothesis that capsaicin-sensitive afferent neurons communicate with postganglionic motoneurons within the bronchus.     

Augmentation of respiratory mast cell secretion of histamine caused by vagus nerve stimulation during antigen challenge

We studied the effect of vagus nerve stimulation on the mast cell secretion of histamine after intraarterial (i.a.) administration of Ascaris suum antigen (AA) into the bronchial circulation of 10 randomly selected, natively allergic dogs in vivo. Respiratory mast cell response was measured as the arteriovenous difference (AVd) in histamine concentration across the bronchus. Plasma histamine concentration was determined simultaneously from right atrium, right ventricle, and femoral artery 60 and 15 sec before and 15, 30, 45, 60, 75, and 90 sec after i.a. injection of sham (Kreb-Henseleit) diluent, 1:100, and 1:30 concentrations of AA. The mean AVd in plasma histamine for five parasympathetically blocked animals (neural blockade with hexamethonium and beta-adrenergic blockade with propranolol) was 1.28 +/- 0.61 ng/ml (sham), 5.16 +/- 19.7 ng/ml (1:100 AA), and 36.6 +/- 11.1 ng/ml (1:30 AA). Substantial augmentation was obtained when AA was administered during parasympathetic stimulation in five other animals (beta-adrenergic blockade, no neural blockade), which was caused by continuous bilateral electrical stimulation of the vagus nerves. A mean AVd in plasma histamine of 110 +/- 27.6 ng/ml was obtained after 1:100 AA (p less than 0.001 vs parasympathetic blockade) and 166 +/- 32.4 ng/ml for 1:30 AA (p less than 0.001 vs parasympathetic blockade). Parasympathetic stimulation alone did not cause secretion of histamine. In contrast to the AVd response, parasympathetic stimulation did not augment nonrespiratory mast cell secretion after AA challenge. We conclude that vagus nerve stimulation augments secretion of histamine from respiratory mast cells during antigen challenge. We demonstrate that parasympathetic stimulation may potentiate the response to antigen challenge in central airways through augmented mast cell secretion of mediator.     

刺激家兔腹部迷走神经外周端引起的降压作用

本文对电刺激家兔腹部的迷走神经外周端所引起的降压反应进行了研究。在121只家兔中的实验结果表明:电刺激腹部迷走神经外周端可引起动脉压、小肠和后肢的灌流压同时降低,而心率则无明显变化。这一降压反应发生时,小肠静脉血中的组织胺含量较刺激前明显升高,然后恢复;将小剂量的组织胺 H_1受体阻断剂扑尔敏、非乃根和 H_2受体阻断剂甲氰咪胍(Cimetidine)分别注入肠系膜上动脉均能减弱刺激腹部迷走神经外周端引起的动脉压和小肠灌流压的降低。心得安能削弱此降压反应,而阿托品无效;切断两侧内脏大神经能显著削弱刺激腹部迷走神经外周端引起的降压反应。此残余的降压反应在注入抗组织胺剂后完全消失。由此推论,刺激家兔腹部迷走神经外周端引起的降压反应是通过中枢和外周两方面因素的作用,使血管舒张,外周阻力降低而实现的。     

Vagal feedback with expiratory threshold load under extracorporeal circulation

In 11 anesthetized dogs placed under extracorporeal circulation, the vagal feedback was tested by electrical stimulation of the vagus nerves with cold block of their caudal part and by passive lung hyperinflation. The apneic response to such vagal stimulation progressively disappeared during expiratory threshold load breathing but then returned to control values some minutes after the load was removed. This suppression of the inhibitory response to stimulation of the vagus nerves was usually observed when vagal afferents were intact or blocked by cold. However, it was not observed whether no evoked activity continued in expiratory muscles after the cold block, or after suppression of all proprioceptive muscular afferents after transection of the spinal cord at C6 level. These results strongly suggest that enhancement of proprioceptive inputs to the respiratory centers counteracts the vagally mediated inspiratory "off-switch" mechanisms.     

Electrical stimulation of afferent vagus nerve induces IL-1beta expression in the brain and activates HPA axis

Possible roles of the afferent vagus nerve in regulation of interleukin (IL)-1beta expression in the brain and hypothalamic-pituitary-adrenal (HPA) axis were examined in anesthetized rats. Levels of IL-1beta mRNA and protein in the brain were measured by comparative RT-PCR and ELISA. Direct electrical stimulation of the central end of the vagus nerve was performed continuously for 2 h. The afferent stimulation of the vagus nerve induced increases in the expression of mRNA and protein levels of IL-1beta in the hypothalamus and the hippocampus. Furthermore, expression of corticotropin-releasing factor mRNA was increased in the hypothalamus 2 h after vagal stimulation. Plasma levels of ACTH and corticosterone were also increased by this stimulation. The present results indicate that activation of the afferent vagus nerves itself can induce production of IL-1beta in the brain and activate the HPA axis. Therefore, the afferent vagus nerve may play an important role in transmitting peripheral signals to the brain in the infection and inflammation.     

Vagus nerve stimulation preferentially induces Fos expression in nitrergic neurons of rat esophagus

To identify neurochemical phenotypes of esophageal myenteric neurons synaptically activated by vagal preganglionic efferents, we immunohistochemically detected the expression of Fos, an immediate early gene product, in whole-mount preparations of the entire esophagus of rats following electrical stimulation of the vagus nerves. When electrical stimulation was applied to either the cervical left (LVN) or right vagus nerve (RVN), neurons with nuclei showing Fos immunoreactivity (IR) were found to comprise approximately 10% of the total myenteric neurons in the entire esophagus. These neurons increased from the oral toward the gastric end of the esophagus, with the highest frequency in the abdominal portion of the esophagus. A significant difference was not found in the number of Fos neurons between the LVN-stimulated and RVN-stimulated esophagus. Double-immunolabeling showed that nitric oxide synthase (NOS)-IR occurred in most (86% and 84% in the LVN-stimulated and RVN-stimulated esophagus, respectively) of the Fos neurons in the entire esophagus. Furthermore, the stimulation of either of the vagus nerves resulted in high proportions (71%-90%) of Fos neurons with NOS-IR, with respect to the total Fos neurons in each segment, in the entire esophagus. However, a small proportion (8% and 7% in the LVN-stimulated and RVN-stimulated esophagus, respectively) of the Fos neurons in the esophagus exhibited choline acetyltransferase (ChAT)-IR. The occurrence-frequency of Fos neurons with ChAT-IR was less than 4% of the total Fos neurons in any segment of the LVN-stimulated and RVN-stimulated esophagus. Some of the Fos neurons with ChAT-IR appeared to be innervated by numerous varicose ChAT-positive nerve terminals. The present results showing that electrical stimulation of the vagus nerves induces a high proportion of Fos neurons with NOS-IR suggests the preferential activation of NOS neurons in the esophagus by vagal preganglionic efferents. This connectivity between the vagal efferents and intrinsic nitrergic neurons might be involved in inhibitory actions on esophageal motility.This study was supported by Grant-in Aids for Scientific Research from Ministry of Education, Sports, and Culture of Japan to H.K. (no. 15500236) and to M.K. (no. 14570065).     

Augmentation of parasympathetic contraction in tracheal and bronchial airways by PGF2 alpha in situ

We studied the effect of exogenous prostaglandin F2 alpha (PGF2 alpha) on airway smooth muscle contraction caused by parasympathetic stimulation in 22 mongrel dogs in situ. Voltage (0-30 V, constant 20 Hz) and frequency-response (0-25 Hz, 25 V) curves were generated by stimulating the cut ends of both cervical vagus nerves. Airway response was measured isometrically as active tension (AT) in a segment of cervical trachea and as change in airway resistance (RL) and dynamic compliance (Cdyn) in bronchial airways. One hour after 5 mg/kg iv indomethacin, a cumulative frequency-response curve was generated in nine animals by electrical stimulation of the vagus nerves at 15-s intervals. Reproducibility was demonstrated by generating a second curve 7 min later. A third frequency-response curve was generated during active contraction of the airway caused by continuous intravenous infusion of 10 micrograms X kg-1 X min-1PPGF2 alpha. Additional frequency-response studies were generated 15 and 30 min after PGF2 alpha, when airway contractile response (delta RL = +2.8 +/- 0.65 cmH2O X 1(-1) X s; delta Cdyn = -0.0259 +/- 0.007 1/cmH2O) returned to base line. Substantial augmentation of AT, RL, and Cdyn responses was demonstrated in every animal studied (P less than 0.01 for all points greater than 8 Hz) 15 min after PGF2 alpha. At 30 min, response did not differ from initial base-line control. In four animals receiving sham infusion, all frequency-response curves were identical. We demonstrate that PGF2 alpha augments the response to vagus nerve stimulation in tracheal and bronchial airways. Augmentation does not depend on PGF2 alpha-induced active tone.     

Canine vagus nerve stores cholecystokinin-58 and -8 but releases only cholecystokinin-8 upon electrical vagal stimulation

Cholecystokinin-58 has been shown to be the major form of cholecystokinin (CCK) released to the circulation upon lumenal stimulation of the small intestine in humans and dogs. In anesthetized dogs, electrical vagal stimulation evokes pancreatic exocrine secretion that is in part mediated through the release of CCK. We studied the molecular form of CCK stored in canine vagus nerves and that released into circulation upon electrical vagal stimulation. Gel filtration and radioimmunoassay of the water and acid extracts of canine vagus nerves indicated CCK-8 (35%) and CCK-58 (65%) as the major molecular forms in the vagus nerve. Both forms of CCK isolated from the vagal extracts were equally bioactive as the standard CCK-8 and CCK-58, respectively, in stimulation of amylase release from isolated rat pancreatic acini. Analysis of plasma collected after electrical vagal stimulation indicated that CCK-8 is the only form released into the circulation. The release of CCK-8 upon electrical vagal stimulation was not affected by application of lidocaine to the upper small intestinal mucosa, suggesting that it was released from vagal nerve terminals.     

Plasma vasopressin response to haemorrhage in the anaesthetized rabbit

In chloralose-urethane anaesthetized rabbits the acute circulatory and plasma vasopressin (pAVP) responses to moderate haemorrhage of 6 mL/kg body weight (10% blood volume) were followed after serial section of the aortic, vagus, and carotid sinus nerves. With all nerves intact, haemorrhage resulted in significant increases in pAVP, accompanied by decreases in systemic arterial pressure and right atrial pressure. With subsequent section of each afferent nerve, pAVP still increased in response to haemorrhage regardless of the order of nerve section. These results suggest that, in the anaesthetized rabbit, there is a further component of the pAVP response to haemorrhage, in addition to those carried in the aortic, vagus, and carotid sinus nerves.     

Parasympathetic cholinergic vasodilator mechanism in the terminal liver microcirculation in rats.

Changes in the diameter of liver sinusoids were studied by an intravital television microscope method in pentobarbital-anaesthetized rats. Dilatation of liver sinusoids was observed during parasympathetic neural stimulation and during acetylcholine administration. Frequency-dependent stimulation-effect relationships were obtained by electrical excitation of intact vagus nerves at supramaximal intensity from 2 to 8 Hz. Acetylcholine concentration-effect relationships were also obtained by intraportal venous infusions of acetylcholine 30 microliter for 5 s from 10(-9) to 10(-2) mol.1(-1). Systemic cholinergic receptor blockade with atropine (1 mg.kg-1) markedly reduced dilatation of liver sinusoids produced by both vagus nerve stimulation and acetylcholine administration. Changes in diameter of liver sinusoids with frequency of neural stimulation and with concentration of administered acetylcholine were also expressed as percentage of observed maximum effect and the respective stimulation-effect curves were constructed such that at a certain percentage of diameter change, the equivalent level of vagus nerve activity was represented by a given concentration of administered acetylcholine. Liver plasma concentration of acetylcholine presumably released during electrical vagal stimulation and reaching liver sinusoids was also estimated and found to be within physiological range. It is therefore proposed that rat liver sinusoids have the capacity for parasympathetic cholinergic vasodilatation.     

Unit responses of the cerebellar cortex to stimulation of the vagus nerve and nerves of the limbs

Responses of 74 cerebellar cortical neurons to electrical stimulation of the vagus nerve and its gastric branches and also of the limb nerves were recorded extracellularly in experiments on rats anesthetized with chloralose and pentobarbital. Phasic and tonic unit responses were similar to all types of stimulation, but fewer neurons responded to stimulation of the vagus nerve than to stimulation of the limb nerves. Monosensory neurons responding only to visceral stimulation, were not found. Among cells giving a phasic response, some had a short and others a long latent period. The latent period of responses of all types was longer to vagal stimulation than to stimulation of the limb nerves. The maximal frequency of rhythmic responses to vagal stimulation was 8/sec, compared with 16/sec for stimulation of the limb nerves. Tonic responses of the neurons were excitatory, inhibitory, and mixed. The type of unit response could vary depending on the frequency and repetitiveness of the stimuli but was otherwise independent of the type of stimulation.N. I. Pirogov Vinnitsa Medical Institute. I. M. Sechenov Institute of Evolutionary Biochemistry and Physiology, Academy of Sciences of the USSR, Leningrad. Translated from Neirofiziologiya, Vol. 4, No. 5, pp. 471–479, September–October, 1972.     

On the purinergic system in rat duodenum: existence of P1 and P2 receptors on the smooth muscle.

In rat duodenum, in vitro, in the presence of atropine and guanethidine, ATP administration caused a tetrodotoxin-insensitive relaxation followed by a rebound contraction. A similar response was obtained also after electrical field stimulation (EFS) of non-adrenergic, non-cholinergic (NANC) nerves. alpha, beta-methylene-TP and theophylline antagonized the response to ATP, but they failed to affect the noradrenaline- and EFS-induced relaxation. These results suggest that P1 and P2 receptors are present in rat duodenum, but their activation is not responsible for the inhibitor effects due to the NANC nerves.     

Neuromodulation of the cardiac vagus: comparison of neuropeptide Y and related peptides

Neuropeptide Y (NPY), a putative co-transmitter in noradrenergic sympathetic nerves of the cardiovascular system, inhibits the negative chronotropic action of the cardiac vagus. In the present study, peptides related to NPY were tested for potency in producing this effect. In bilaterally vagotomized, anaesthetised dogs, the increase in pulse interval caused by electrical stimulation of the peripheral stump of the right vagus was measured before and after intravenous administration of peptide. The effects of doses of NPY were compared with those of equimolar doses of peptide YY (PYY), and of avian and human pancreatic polypeptides (APP and HPP). PYY inhibited the vagal action more effectively than did NPY. APP and HPP, however, caused no change in strength of vagal action at the doses used. The response to a second injection of NPY, given soon after the injection of APP or HPP, was not significantly different from the original. Thus no evidence was obtained for a competitive inhibition of the action of NPY by either pancreatic polypeptide. A C-terminal hexapeptide fragment of human pancreatic polypeptide was also tested. Like APP and HPP, it neither inhibited the cardiac vagus nor blocked the action of NPY. The order of potency obtained here (PYY greater than NPY much greater than APP, HPP, CFPP) can be expected to be of use in efforts to distinguish the active site(s) of the NPY molecule, and to characterise the receptors involved in these modulatory effects.     

Autonomic response characteristics of porcine airway smooth muscle in vivo

We studied the autonomic response characteristics of airways in 65 swine in vivo. Tracheal smooth muscle response was measured isometrically in situ; bronchial response was measured simultaneously as change in airway resistance and dynamic compliance. To determine the optimal resting length at which maximal tracheal contraction was obtained, length-tension studies were generated in four animals using maximal electrical stimulation of the vagus nerves determined from stimulus-response characteristics in eight other swine. Pharmacological studies were performed in 25 animals to determine the relative potency and intrinsic activity of agonists (acetylcholine greater than histamine much greater than norepinephrine) causing contraction of trachea and bronchial airways. In 13 swine, the effects of autonomic stimulation were studied by intravenous administration of dimethylphenylpiperazinium (DMPP) after muscarinic blockade with 1.5 mg/kg iv atropine. Tracheal contraction caused by topical application of 3.4 X 10(-4) mol histamine (13.4 +/- 1.54 g/cm) was 96 +/- 7.2% blocked by 25 micrograms/kg iv DMPP in adrenal-intact animals; minimal relaxation was demonstrated in adrenalectomized animals, indicating absence of substantial sympathetic innervation to porcine trachea. Nonadrenergic innervation was not demonstrated. After beta-adrenergic blockade, sympathetic stimulation caused alpha-adrenergic contraction in bronchial airways but not in trachea. These data define the unique response characteristics of the airways of swine and demonstrate their utility for acute experimental study of airway responses in vivo.     

The role of vagus nerves in different changes of the right atrial pressure following intravenous injection of pressor vasoactive drugs

In acute experiments on anesthetized cats, intravenous injection of the norepinephrine and angiotensin caused different changes of right atrial pressure in intact animals (decreasing--I group, of animals, and increasing--II group). After right and left vagus nerves had been cut, the right atrial pressure in the I group of animals decreased, but its changes were lesser than in intact animals due to slowing down of the increase of the right ventricular myocardial contractility and venous return. The latter was the result of severe diminution of the increase of the superior vena cava flow compared with the intact animals, meanwhile the value of the inferior vena cava flow did not change. In the II group animals after vagotomy and intravenous injection of the noripinephrine and angiotensin the sign of the right atrial pressure became negative, i. e. the direction of its shifts changed to the opposite, compared with intact animals. In this case, the changes of the sign of the right atrial pressure was caused by the removal of the reflectory inhibitory vagal influences on the heart, because the values of the right ventricular myocardial contractility and venous return were the same as in intact animals of the group, due to decreasing of the value of the superior vena cava flow and increasing of the shifts of the inferior vena cava flow. The vagotomy alone caused also different changes (decreasing or increasing) of right atrial pressure following increasing of the right ventricular myocardial contractility, meanwhile the changes of the venous return were insignificant. Direct electrical stimulation of both the right and the left vagus nerves caused the increasing of the right atrial pressure and decreasing of the right ventricular myocardial contractility and venous return. Thus we concluded, that different changes of the right atrial pressure in animals following intravenous injection of the pressor vasoactive drugs could be the result of different manifestations of the vagal afferent impulsation, which has influence on the sympathetic tonic discharges on the vessels of the regions of the superior and inferior vena cava, and the vagal reflectory inhibitory influences on the heart.     

The superior laryngeal nerve and the superior laryngeal artery

Length, diameter and anastomoses of the nervus vagus and its ganglion inferius were measured 44 halved heads. On the average, 8.65 fiber bundles of the vagus nerve leave the retro-olivary area. In the area of the jugular foramen is the near superior ganglion of the 10th cranial nerve. In this area were found 1.48 (mean value) anastomoses with the 9th cranial nerve. 11.34 mm below the margo terminalis sigmoidea branches off the ramus internus of the accessory nerve which has a length of 9.75 mm. Further anastomoses with the 10th cranial nerve were found. The inferior ganglion of the 10th nerve had a length of 25.47 mm and a diameter of 3.46 mm. Five mm below the ganglion the 10th nerve had a width of 2.9 and a thickness of 1.5 mm. The mean length of the superior sympathetic ganglion was 26.6 mm, its width 7.2 and its thickness 3.4 mm. In nearly all specimens anastomoses of the superior sympathetic ganglion with the ansa cervicalis profunda and the inferior ganglion of the 10th cranial nerve were found. The superior laryngeal nerve branches off about 36 mm below the margo terminalis sigmoidea. The width of this nerve was 1.9 mm, its thickness 0.8 mm on the right and 1.0 mm on the left side. The division in the internal and external rami was found about 21 mm below its origin. Between the n. vagus and thyreohyoid membrane the ramus internus had a length of 64 mm, the length of external ramus between the vagal nerve and the inferior pharyngeal constrictor muscle was 89 mm. Its mean length below the thyreopharyngeal part was 10.7 mm, 8.6 branchlets to the cricothyroid muscle were counted. The superior laryngeal artery had its origin in 80% of cases in the superior thyroideal artery, in 6.8% this vessel was a branch of the external carotid artery. Its average outer diameter was 1.23 mm on the right side and 1.39 mm on the left. The length of this vessel between its origin and the thyreohyoid membrane was 34 mm. In 7% on the right side and in 13% on the left, the superior laryngeal artery reached the larynx through a foramen thyreoideum. Ranges of diameters and lengths of vessels and nerves in the larynx are given.