Synaptic transmission in thoracic autonomic ganglia of the dog

Afferent stimulation of one canine thoracic cardiopulmonary nerve can generate compound action potentials in another ipsilateral cardiopulmonary nerve. These compound action potentials persist after acute decentralization of the middle cervical ganglion, indicating that they result from neural activity in the middle cervical ganglion and thoracic nerves. Changing the frequency of stimulation can alter the compound action potentials, suggesting that temporal facilitation or inhibition occurs in this middle cervical ganglion preparation. The compound action potentials can be modified by stimulation of sympathetic preganglionic fibers and by hexamethonium, atropine, phentolamine, propranolol, and (or) manganese. It thus appears that afferent cardiopulmonary nerves can activate efferent cardiopulmonary nerves via synaptic mechanisms in the stellate and middle cervical ganglia. It also appears that these mechanisms involve adrenergic and cholinergic receptors and are influenced by preganglionic sympathetic fibers arising from the cord.     

Effects of Neuronal Activity on Inositol Phospholipid Metabolism in the Rat Autonomic Nervous System

The effect of nerve stimulation on inositol phospholipid hydrolysis in autonomic tissue was assessed by direct measurement of [3H]inositol phosphate production in ganglia that had been preincubated with [3H]inositol. Within minutes, stimulation of the preganglionic nerve increased the [3H]inositol phosphate content of the superior cervical sympathetic ganglion indicating increased hydrolysis of inositol phospholipids. This effect was blocked in a low Ca2+, high Mg2+ medium. It was also greatly reduced when nicotinic and muscarinic antagonists were present together in normal medium. However, neither the nicotinic antagonist nor the muscarinic antagonist alone appeared to be as effective as both in combination. In other experiments, stimulation of the vagus nerve caused dramatic increases in [3H]inositol phosphate in the nodose ganglion but did not increase [3H]inositol phosphate in the nerve itself. This effect was insensitive to the cholinergic antagonists. Thus, neuronal activity increased inositol phospholipid hydrolysis in a sympathetic ganglion rich in synapses, as well as in a sensory ganglion that contains few synapses. In the sympathetic ganglion, synaptic stimulation activated inositol phospholipid hydrolysis and this was primarily due to cholinergic transmission; both nicotinic and muscarinic pathways appeared to be involved.     

Functional and anatomical variability of canine cardiac sympathetic efferent pathways: implications for regional denervation of the left ventricle

To further elucidate the functional anatomy of canine cardiac innervation as well as to assess the feasibility of producing regional left ventricular sympathetic denervation, the chronotropic and (or) regional left ventricular inotropic responses produced by stellate or middle cervical ganglion stimulation were investigated in 22 dogs before and after sectioning of individual major cardiopulmonary or cardiac nerves. Sectioning the right or left subclavian ansae abolished all cardiac responses produced by ipsilateral stellate ganglion stimulation. Sectioning a major sympathetic cardiopulmonary nerve, other than the right interganglionic nerve, usually reduced, but seldom abolished, regional inotropic responses elicited by ipsilateral middle cervical ganglion stimulation. Sectioning the dorsal mediastinal cardiac nerves consistently abolished the left ventricular inotropic responses elicited by right middle cervical ganglion stimulation but minimally affected those elicited by left middle cervical ganglion stimulation. In contrast, cutting the left lateral cardiac nerve decreased the inotropic responses in lateral and posterior left ventricular segments elicited by left middle cervical ganglion stimulation but had little effect on the inotropic responses produced by right middle cervical ganglion stimulation. In addition, the ventral mediastinal cardiac nerve was found to be a significant sympathetic efferent pathway from the left-sided ganglia to the left ventricle. These results indicate that the stellate ganglia project axons to the heart via the subclavian ansae and thus effective sympathetic decentralization can be produced by cutting the subclavian ansae; the right-sided cardiac sympathetic efferent innervation of the left ventricle converges intrapericardially in the dorsal mediastinal cardiac nerves; and the left-sided cardiac sympathetic efferent innervation of the left ventricle diverges to innervate the left ventricle by a number of nerves including the dorsal mediastinal, ventral mediastinal, and left lateral cardiac nerves. Thus consistent denervation of a region of the left ventricle can not be accomplished by sectioning an individual cardiopulmonary or cardiac nerve because of the functional and anatomical variability of the neural components in each nerve, as well as the fact that overlapping regions of the left ventricle are innervated by these different nerves.     

Cardiac effects produced by long-term stimulation of thoracic autonomic ganglia or nerves: implications for interneuronal interactions within the thoracic autonomic nervous system

Electrical stimulation of an acutely decentralized stellate or middle cervical ganglion or cardiopulmonary nerve augments cardiac chronotropism or inotropism; as the stimulation continues there is a gradual reduction of this augmentation following the peak response, i.e., an inhibition of augmentation. The amount of this inhibition was found to be dependent upon the region of the heart investigated and the neural structure stimulated. The cardiac parameters which were augmented the most displayed the greatest inhibition. Maximum augmentation or inhibition occurred, in most instances, when 5-20 Hz stimuli were used. Inhibition of augmentation was overcome when the stimulation frequency was subsequently increased or following the administration of nicotine or tyramine, indicating that the inhibition was not primarily due to the lack of availability of noradrenaline in the nerve terminals of the efferent postganglionic sympathetic neurons. Furthermore, as infusions of isoproterenol or noradrenaline during the period of inhibition could still augment cardiac responses, whereas during the early peak responses they did not, the inhibition of augmentation does not appear to be due primarily to down regulation of cardiac myocyte beta-adrenergic receptors. The inhibition was modified by hexamethonium but not by phentolamine or atropine. Inhibition occurred when all ipsilateral cardiopulmonary nerves connected with acutely decentralized middle cervical and stellate ganglia were stimulated, whereas significant inhibition did not occur when these nerves were stimulated after they had been disconnected from the ipsilateral decentralized ganglia. Taken together these data indicate that the inhibition of cardiac augmentation which occurs during relatively long-term stimulation of intrathoracic sympathetic neural elements is due in large part to nicotinic cholinergic synaptic mechanisms that lie primarily in the major thoracic autonomic ganglia. They also indicate that long-term stimulation in intrathoracic sympathetic neural elements with frequencies as low as 2 Hz may augment the heart as much as higher stimulation frequencies, depending upon the structure stimulated and the cardiovascular parameter monitored.     

Electrical activity of the sympathetic ganglia during the depressor reflex

Tonic activity of neurons of the superior cervical sympathetic ganglion was recorded by the "sucrose gap" method and in the 4th and 5th lumbar sympathetic ganglia with the aid of focal nonpolarizing electrodes in acute experiments on anesthetized cats and rabbits. The preganglionic fibers of the ganglia were left intact. Stimulation of the depressor nerve not only sharply inhibited the tonic activity of the ganglia but also led to the appearance of electropositive potentials of 0.7 ± 0.2 mV in the superior cervical ganglion and 20–250 µV in the lumbar ganglia. The amplitude of this potential was unchanged by atropine (1 · 10^–6M). A similar effect occured without stimulation of the depressor nerve, after division of the preganglionic fibers or blocking of their conduction; it is attributed to the cessation of preganglionic tonic impulses which induce not only spikes, but also many EPSPs in neurons of the ganglion. Their frequency in the lumbar ganglia was 4/sec. Summation of these EPSPs leads to constant electronegativity of the ganglion surface relative to the postganglionic fibers, and its disappearance is recorded as a positive potential. Stimulation of the depressor nerve thus does not induce IPSPs in the ganglion; consequently, the inhibition of synaptic activity observed under these circumstances is located in the CNS and not in the ganglion.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 6, No. 5, pp. 519–524, September–October, 1974.     

Changes in ventricular fibrillation threshold with stimulation of cardiac sympathetic nerves of the developing dog

The effect of stimulation of the developing cardiac sympathetic nerves on the vulnerability to ventricular fibrillation was investigated in 50 puppies 1 to 6 weeks of age. Ventricular fibrillation thresholds were obtained before and during sympathetic nerve stimulation. Stimulation of either stellate ganglion increased ventricular fibrillation threshold, possibly due to diffuse functional innervation in pups. The effect of the left stellate increased progressively with age, whereas the effect of the right, although initially greater than that of the left, did not increase further with age. In contrast, stimulation of the left ventrolateral cardiac nerve, which is locally distributed, resulted in decreased ventricular fibrillation threshold. This decrease was progressively greater with age. The fact that activation of the left stellate ganglion and the left ventrolateral cardiac nerve affects ventricular fibrillation threshold in opposite directions suggests different sympathetically mediated changes on ventricular vulnerability in early life. The differing temporal patterns of maturation and the localized nature of the major distal branch distributions could provide a mechanism for promotion of arrhythmiogenesis under some conditions in early life.     

Occurrence of parasympathetic vasodilator fibers in the lower lip of the guinea-pig

The present study was designed to examine whether there are parasympathetic vasodilator fibers in the lower lip of the guinea-pig. Electrical stimulation of the central cut end of the lingual nerve of guinea-pigs evoked intensity- and frequency-dependent decreases in lower lip blood flow and systemic arterial blood pressure (SABP). Pretreatment with guanethidine, a postganglionic sympathetic nerve blocker and antihypertensive drug (30 mg kg⁻¹, s.c., 24 h prior to experiments), reduced the magnitude of the decrease in SABP while the intensity- and frequency-dependent increases of the lip blood flow occurred by the lingual nerve stimulation only on the side ipsilateral to stimulation. Increases in the lip blood flow evoked by lingual nerve stimulation in guanethidine pretreated guinea-pigs were reduced by hexamethonium (an autonomic ganglion cholinergic blocker) in a dose-dependent manner. When fluoro-gold (a retrograde neural tracer) was injected into the lower lip, labeled neurons were observed in the ipsilateral otic ganglion. The present study indicates the presence of parasympathetic vasodilator fibers originating from the otic parasympathetic ganglion in the guinea-pig lower lip, similar to those reported previously in rats, cats, rabbits and humans.     

The effects of morphine on sympathetic transmission in the stellate ganglion of the cat

The aim of this study was to investigate which of the processes involved in synaptic transmission are affected by morphine in concentrations comparable to those used during surgical procedures. The effects of morphine sulfate on ganglionic transmission were studied in the stellate ganglion of the cat using intracellular and extracellular recordings in vitro. The neurons of the stellate ganglion were depolarized using preganglionic nerve stimulation, postganglionic nerve stimulation, and intracellular stimulation before and after introduction of morphine sulfate (up to 20 micrograms/mL). Tissue concentrations of morphine were estimated using radiolabeled morphine. Axonal transmission and the excitability of the postganglionic neurons to direct intracellular stimulation was not affected at the concentrations of morphine studied. In addition, morphine had a dose-dependent depolarizing effect on the resting membrane potential of most of the neurons in the stellate ganglion. Such neuronal depolarizations alone could initially produce excitation in some cell populations, followed by inhibition, secondary to the membrane depolarization, leading to depression of sympathetic nerve activity. The overall ganglionic transmission as recorded using an evoked potential was biphasic. At low doses morphine facilitated transmission, while at larger doses morphine attenuated evoked potentials. These effects do not appear to be mediated through classical opiate receptors since they are not blocked by naloxone.     

Mechanism of the intracardiac interactions of the vagus and sympathetic nerves: is a serotoninergic mechanism possible?

A study was made of the conditions of the occurrence and mechanisms of the enhancement by the sympathetic nerve of the vagus-induced inhibition of rabbit heart work. It was discovered that to obtain such a phenomenon, it is necessary that stimulation of the stellate ganglion be made in the presence of perithreshold stimulation of the vagus after blockade of beta-adrenoreceptors. The inhibitory effect was not abolished by dihydroergotoxin but was blocked by promedol, aminazine and diprazine. It is suggested that the serotoninergic component is involved in the mechanism of the enhancement of the vagus-induced inhibition that occurs during stimulation of the sympathetic nerve.     

Modulation of reflexsympathetic discharge by the cholinergic agonist oxotremorine and by clonidine

The cholinergic agonist oxotremorene can produce marked centrally-mediated cardiovascular effects. In past experiments in anesthetized cats, oxotremorine reduced blood pressure and an evoked sympathetic reflex. However, unlike other sympathetic inhibitors, it decreased sympathetic outflow selectively, did not slow heart rate but prolonged the latency of an evoked sympathetic reflex. In view of these striking differences, effects of oxotremorine on another reflex involved in cardiovascular control were assessed in anesthetized cats and compared to those produced by clonidine. Stimulation of the carotid sinus nerve with short duration pulses evoked reflex firing in the splanchnic nerve. Oxotremorine (50 – 800 ug/kg i.v.) caused a dose-related decrease in blood pressure and inhibited the evoked potential at the higher doses (200–800 ug/kg) but did not prolong its latency. Clonidine produced similar effects. Thus, attenuation by oxotremorine of an additional fundamental cardiovascular reflex was demonstrated. Seletcive inhibition of sympathetic outflow by oxotremorine as well as its differential effect on the latencies of cardiovascular reflexes indicates that the compound influences medullary and descending sympathetic pathways in a complex manner and suggests that the inhibition occurs at more than one site.     

Neuropeptide Y (NPY) and the pig heart: release and coronary vasoconstrictor effects

The effects of electrical stimulation of the stellate ganglia on the arterio-venous concentration differences of neuropeptide Y (NPY)-like immunoreactivity (LI) over the pig heart were studied in vivo in relation to changes in heart rate and left ventricular pressure. Furthermore, the effects of NPY on coronary vascular tone were analysed in vivo and in vitro. Stellate ganglion stimulation at a high frequency (10 Hz) caused a clear-cut, long lasting increase in plasma levels of NPY-LI in the coronary sinus compared to the aorta, suggesting release of this peptide from sympathetic terminals within the heart. The stimulation-evoked overflow of NPY-LI from the heart was enhanced about 3-fold by alpha-adrenoceptor blockade using phenoxybenzamine, suggesting that NPY release is under prejunctional inhibitory control by noradrenaline (NA). Combined alpha- and beta-adrenoceptor blockade abolished most of the positive inotropic response of the heart upon stellate ganglion stimulation, while a considerable positive chronotropic effect remained. After guanethidine treatment, stellate ganglion stimulation still produced a small positive inotropic and chronotropic effect on the heart. The stimulation evoked NPY overflow was markedly reduced by guanethidine indicating an origin from sympathetic nerve terminals. Injection of NPY into the constantly perfused left anterior descending artery in vivo caused a long lasting, adrenoceptor antagonist resistant increase in perfusion pressure, suggesting coronary vasoconstriction. NPY contracted coronary arteries in vitro via a nifedipine-sensitive mechanism. NA dilated coronary vessels both in vivo and in vitro via beta-adrenoceptor activation. It is concluded that sympathetic nerve stimulation increases overflow of NPY-LI from the heart suggesting release from cardiac nerves in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)     

Functional anatomy of canine cardiac nerves.

In 20 anesthetized dogs the thoracic autonomic nerves were carefully exposed in order to determine which produced cardiovascular responses when the afferent or efferent component of each was stimulated. Efferent parasympathetic and sympathetic fibers arise from the caudal cervical ganglion regions bilaterally as well as from the vagus caudally to that ganglion. The majority of negative chromotropic, dromotropic and inotropic fibers arise from the vagus or near the recurrent laryngeal nerves; however, some small parasympathetic fibers also arise from the vagi down to the level of the pulmonary vessels. Efferent sympathetic nerves are relatively large with the exception of the stellate cardiac nerves, and produce specific positive chronotropic or inotropic responses. Afferent fibers are numerous in the recurrent cardiac, innominate, ventromedial and dorsal nerves and not very numerous in both stellate cardiac nerves as well as in the nerves at the level of the pulmonary vessels; thus there are numerous cholinergic and adrenergic efferent fibers which exhibit specific chronotropic or inotropic responses. The correlation between neural anatomy and specific physiological cardiodynamics illustrates beautifully the interrelationship of structure and function which exists within the autonomic nervous system.     

Tonic impulsation in preganglionic and postganglionic sympathetic fibers of mammals

A study of the tonic electrical activity of nerves containing preganglionic and postganglionic fibers in the superior cervical and stellate sympathetic ganglia of cats and rabbits has shown that this activity consists of groups of spikes synchronous with the pulse or respiration, and occurs on a background of irregular low-amplitude impulses. The frequency of spikes is higher (250/sec) in nerves containing preganglionic fibers than in those containing postganglionic fibers (100/sec). Groups of spikes in a nerve containing preganglionic fibers correspond in some preparations to groups of spikes of lower frequency in a nerve containing postganglionic fibers of the same ganglion; in other preparations, this correspondence was lacking, apparently due to the absence of synaptic contacts between those groups of pre- and postganglionic neurons whose activity was recorded. Neurons send axons to different nerves (cardiac and vertebral) of the stellate ganglion discharged synchronously in some preparations, and asynchronously in others. Where synchronization was observed, the neurons discharged in rhythm with cardiac contractions.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 1, No. 3, pp. 303–308, November–December, 1969.     

Conducting pathways of the superior cervical sympathetic ganglion of the cat

Individual nerves of the superior cervical sympathetic ganglion were stimulated in acute experiments on cats, and action potentials (AP) were recorded from other nerves of the ganglion in order to clarify whether or not there is transmission of excitation through the ganglion from one nerve to another and to establish whether this transmission is continuous or synaptic. The method of intracellular recording from neurons of the ganglion was also used. It is established that stimulation of the cervical sympathetic nerve evokes AP in all of the peripheral nerves of the ganglion, a circumstance that is the result of synaptic transmission of excitation. There is no transmission of excitation in the reverse direction or between any of the 12 peripheral nerves of the ganglion (including the four branches of the internal carotid nerve). Orthodromic excitation is recorded intracellularly from neurons of the ganglion during stimulation of the cervical sympathetic nerve, and antidromic excitation is recorded during stimulation of a peripheral nerve (the internal carotid nerve). It follows that the pathways through the ganglion which conduct excitation from the cervical sympathetic nerve into all of the remaining nerves of the ganglion are synaptic. Analysis of EPSP latent periods indicated that preganglionic fibers that differ sharply with respect to threshold and conduction rate (groups S₂ and S₄) converge on one and the same neurons of the ganglion.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 2, No. 2, pp. 216–224, March–April, 1970.     

Cardioacceleration produced by close intra-arterial injection of neurotensin into the stellate ganglion of the cat

The effect on heart rate of close i.a. injection of neurotensin (NT), substance P (SP), and vasoactive intestinal peptide (VIP) into the decentralized right stellate ganglion was tested in anaesthetized spinal cats. These peptides are present in the stellate ganglion and may mediate the stellate ganglion cell excitation underlying a previously described slow cardioacceleration evoked by preganglionic stimulation during block of cholinergic transmission. NT (Tyr11-NT) at doses of 25-200 micrograms produced increases in heart rate of 10-125 beats/min (bpm) and of slow time course. At the dose of 100 micrograms, NT produced a cardioacceleration of 56 +/- 8.4 bpm (mean +/- SEM, n = 13) with an onset latency of 23 +/- 4 s, a slow rise to peak (rise time 62 +/- 4.5 s), and a half decay of 167 +/- 14 s. A cardioacceleration of comparable magnitude (78 +/- 3.8 bpm) caused by close i.a. administration of acetylcholine (100 micrograms, n = 13) had an onset latency of 2 +/- 1 s, a fast rise to a sharp peak (rise time 3 +/- 1 s), and a half decay of 23 +/- 4 s. The analogues, Phe11-NT and Trp11-NT, as well as the stereoisomer, D-Tyr11-NT, had no effect on heart rate when injected at doses up to 400 micrograms. The NT-evoked cardioacceleration was blocked by propranolol or by section of the inferior cardiac nerve and may therefore be attributed to prolonged excitation of stellate ganglion cells. Administration of hexamethonium and atropine was without effect on the NT response.(ABSTRACT TRUNCATED AT 250 WORDS)     

The autonomic innervation of the ovary of the dab,Limanda yokohamae

The autonomic innervation of the ovary of the dab was studied histologically and physiologically. The ovary receives a branch of nerve bundles that emerge into the abdominal cavity at the postero-ventral end of the kidney and can be traced back to the sympathetic chain in the vicinity of the 5th vertebra. Almost all the nerve fibers are AChE-positive, and some of them also emit adrenergic fluorescence. Electrical stimulation of the ovarian nerves caused ovarian contractions, and administration of ACh elicited contractions of the ovary preparations, supporting the hypothesis that the ovary is innervated by excitatory cholinergic fibers. In the ovarian nerve bundles, many AChE-positive and non-fluorescent ganglion cells are scattered. Ultrastructural studies suggest that nerve endings situated on the ovarian smooth muscle and on ganglion cells are cholinergic. These results also suggest that the cells are the post-ganglionic neurons of the cholinergic innervation and the axons of the cells reach to the muscle cells. On the other hand, the adrenergic fluoresecent fibers possibly participate in the inhibitory innervation, since the presence of inhibitory beta-adrenoceptors were demonstrated by pharmacological studies.     

Hypothalamic modulation of baroreceptor inhibition of the electrical activity in the renal nerve

Changes in the renal nerve sympathetic activity in response to electrical stimulation of posterior hypothalamus and vago-aortic nerve were studied in acute experiments on cats. It was shown that stimulation of certain points in hypothalamus defence area led to the suppression of baroreceptor reflex-mediated inhibition of the renal nerve sympathetic activity. Chloralosa depressed hypothalamic modulation of baroreceptor reflexes.     

星状神经节电刺激建立交感神经介导的急性房颤犬模型

目的建立交感神经张力异常介导的急性房颤动物模型的方法学。方法将16只随意来源犬分为三组：对照组（n=4）,右侧星状神经节（aSG）组（n=6）和左侧星状神经节（LSG）组（n=6）,测定心房和肺静脉不同部位的房颤诱发率、房颤持续时间。结果RSG刺激显著增加右心房（RA）的房颤诱发率和持续时间（P〈0．05）,LSG刺激显著增加左心房（LA）、左上肺静脉（LSPV）、左下肺静脉（LIPV）的房颤诱发率和持续时间（P〈0．05）;与刺激时相比,RSG切除显著降低RA的房颤诱发率和持续时间（P〈0．05）;LSG切除显著降低LA、LSPV、LIPV的房颤诱发率和持续时间（P〈0．05）。结论星状神经节电刺激同时快速心房起搏6h可成功建立交感神经介导的急性房颤犬模型,星状神经节电刺激使心房和肺静脉部位的房颤诱发率显著升高,房颤持续时间显著延长,去星状神经节支配可减少房颤的发生和维持。     

CGRP-immunoreactive sensory nerve fibers in the submandibular gland of the rat

Summary Indirect immunofluorescence technique was used to study the occurrence and distribution of CGRP immunoreactivity in the submandibular gland of normal rats and after unilateral sensory and sympathetic denervations. In normal rats, CGRP-immunoreactive nerve fibers and nerve trunks were seen around or in close contact with interlobular salivary ducts as well as around small blood vessels of the gland. Occasionally, CGRP-immunoreactive nerve fibers were also detected between or around the acini of the gland.The submandibular ganglia contained CGRP-immunoreactive nerve fibers, but the ganglion cells were not immunoreactive for CGRP. The trigeminal ganglion contained a population of CGRP-immunoreactive, mainly small sized ganglion cells and nerve fibers distributed throughout the ganglion. Unilateral electrocoagulation of the trigeminal nerve caused a significant reduction in the number of immunoreactive nerve fibers in the gland, although some fibers still were present in the ipsilateral glandular tissue. Unilateral superior cervical ganglionectomy caused no detectable effect on the number of CGRP-immunoreactive nerve fibers in the gland.The present results suggest that the rat submandibular gland contains CGRP-immunoreactive nerve fibers both around blood vessels and in glandular secretory elements. Denervation experiments support the view that the majority, but perhaps not all of them originate from the trigeminal ganglion.     

Mapping of ventricular tachycardia induced by thoracic neural stimulation in dogs

To investigate ventricular tachycardias produced in healthy canine myocardium by stimulation of sympathetic ganglia or cardiac nerves, we simultaneously recorded a surface ECG and 63 ventricular electrograms in anesthetized open-chest dogs. Isochronal and isopotential maps were generated off-line by computer. Ventricular tachycardia with uniform beat-to-beat morphology was induced in 13 or 22 dogs by electrical stimulation of the left stellate ganglion (five experiments), the left middle cervical ganglion (four experiments), the left caudal pole cardiopulmonary nerve (two experiments), or the ventrolateral cardiac nerve (eight experiments). It was not inducible by stimulation of the right-sided major cardiopulmonary nerves or ganglia. In most instances the earliest measured electrical excitation occurred on the posterior aspect of the ventricles. Isochronal maps demonstrated a radial spread of the impulse away from the area of earliest excitation. Changes in the region of earliest excitation and (or) activation pattern were accompanied by changes in QRS morphology. The potential gradients measured between areas displaying positive and negative T waves on the anterior and left lateral aspects of the ventricles were significantly increased by ventrolateral cardiac nerve stimulation. However, the ventricular regions where these potential gradients existed differed from the regions of earliest excitation during ventricular tachycardia. These results demonstrate that the thoracic autonomic nervous system can induce repetitive ventricular excitation originating from consistent loci.