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PubMed1988

Delayed afterdepolarizations elicited in vivo by left stellate ganglion stimulation.

Activation of cardiac sympathetic nerves is recognized as a triggering factor for cardiac arrhythmias. However, the mechanisms involved have only been speculated. Because evidence from studies in vitro has established a relation between catecholamines, delayed afterdepolarizations (DAD), and triggered rhythms, it seemed possible that in vivo adrenergic activation also might lead to the development of DAD. Because very little evidence was available for DAD in vivo, we have evaluated whether monophasic action potential (MAP) recording with a contact electrode could be a suitable technique for the detection of DAD from the endocardium of anesthetized cats. In six animals, atrial pacing and graded aortic constriction were performed during MAP recording to assess MAP stability during hemodynamic changes, and in no cases were modifications of the baseline observed. In 11 cats, calcium gluconate (0.5 g) and G-strophanthin (100 micrograms) were administered. Action potential duration at 50% (APD50) and 90% (APD90) repolarization were reduced (from 138 +/- 16 to 122 +/- 18 msec, p less than 0.02, and from 163 +/- 23 to 149 +/- 20 msec, p less than 0.025, respectively). In eight of 11 (73%) animals, DAD were elicited with a mean amplitude of 1.2 +/- 0.4 mV. In 14 cats, the left stellate ganglion was stimulated for 45 seconds. APD50 and APD90 decreased (from 153 +/- 15 to 145 +/- 16 msec, p less than 0.005, and from 176 +/- 18 to 165 +/- 13 msec, p less than 0.001, respectively). DAD were induced in 10 of 14 animals (71%) with a mean amplitude of 1.2 +/- 0.3 mV. These results show that DAD can be induced in vivo by administration of calcium and digitalis and by activation of the cardiac sympathetic nerves. This latter finding further strengthens the existing link between adrenergic activation and ventricular arrhythmogenesis and suggests triggered activity as a likely mechanism.

Action Potentials↗
PubMed1962

A ganglion stimulating action of neostigmine.

The actions of neostigmine on transmission in the superior cervical ganglion have been investigated by means of the nictitating membrane preparation in the anaesthetized cat. Intravenous injections of neostigmine produced a rapid and often complete reversal of hexamethonium block, whereas eserine had no effect. This reversal by neostigmine was obtained regularly even after large doses of eserine or dyflos, but was sometimes brief. In ganglia perfused with heparinized plasma containing neostigmine (10(-8) to 10(-4)), there was no potentiation of the responses to maximal stimulation of the preganglionic nerve. Intra-arterial injections of neostigmine to both normal and preganglionically denervated ganglia produced first a potentiation of the responses to nicotine, then, with larger doses, a contraction of the nictitating membrane and, concurrently, a depression of the responses to nicotine. These results are consistent with the view that neostigmine exerts a direct stimulant action on the ganglion, which is distinct from its anticholinesterase action.

Animals↗
PubMed1994

[Influence of superior cervical ganglion stimulation of vestibular function].

The sympathetic nervous system, which originates in the superior cervical ganglion (SCG) and is distributed in vestibular end organs, has been proposed to have some influence on vestibular function. The present investigation was conducted to assess the effects of unilateral electrical stimulation of the SCG, administration of a vasopressor drug, and introduction of KCl (0.7 M/ml) into the tympanic cavity on vestibular function in alert guinea pigs. Nystagmus was not observed as result of electrical irritation of the SCG (22 test animals), infusion of the KCl solution into the middle ear cavity (5 test animals), or the combination of SCG stimulation and vasopressor drug administration (7 test animals). However, when the SCG was stimulated electrically after introduction of the KCl solution into the ipsilateral cavity, nystagmus and postural deviation were observed (5 out of 12 animals). Furthermore, after the administration of a vasopressor drug to these 12 animals, irrespective of the manifestation of nystagmus, the same changes took place in response to the electrical stimulation (7 animals). These results suggest that SCB stimulation is a provocative factor for nystagmus, that infusion of KCl solution into the tympanic cavity induces a hypersensitive state in the inner ear, and that high blood pressure increases this hypersensitivity.

Animals↗
PubMed1988

Coronary sinus norepinephrine concentrations during ventricular tachycardia induced by left stellate ganglion stimulation in dogs.

Coronary sinus catecholamine overflow was measured in open-chest dogs, anesthetized with sodium thiopental and alpha-chloralose, during left sympathetic stimulation. Uniform ventricular tachycardias were induced in 9 out of 16 dogs during either left stellate ganglion or left ventrolateral cardiac nerve stimulations. Significant increases in norepinephrine (8.1 ng/mL, plasma) and epinephrine (0.19 ng/mL, plasma) overflows were obtained after 30 and 90 s of stimulation, respectively. Maximum norepinephrine overflow was significantly higher in dogs with ventricular tachycardia than in those without it (16.0 vs. 7.4 ng/mL, p less than 0.05). This suggests that the induction of ventricular tachycardia in the normal myocardium is related to the amount of local secretion of norepinephrine during nerve stimulation.

Animals↗
PubMed1991

Insulin stimulates ganglionic protein synthesis and reduces thymidine incorporation in support cells of the in vitro regenerating adult frog sciatic sensory neurons.

Insulin was tested for effects on crush injured, in vitro regenerating, adult frog sciatic sensory axons. A wide range of insulin concentrations (0.01-10 micrograms x ml-1) was found to stimulate incorporation of radioactive leucine into ganglionic protein by 50-80%, without affecting the regeneration distance. Simultaneously insulin inhibited the proliferation of the support cells at the crush region by 30%, as measured by thymidine incorporation. Experiments using compartmentalized culture dishes indicated that the proliferation inhibitory effect could be indirect and mediated by the neuronal cells. The results suggest that insulin influences the metabolism of adult peripheral neuronal cell bodies. The stimulated nerve cells could in turn affect the proliferation of support cells in the nerve trunk.

Animals↗
PubMed1987

Central neuronal responsiveness to sensory ganglion stimulation is correlated with the incidence of spontaneous bioelectric activity in developing spinal cord cultures.

In spinal cord explants co-cultured with dorsal root ganglion cells for 3-4 weeks in a (horse)serum-containing medium, the spread of ganglion-evoked action potentials from monosynaptic innervation sites ("polysynaptic excitability index") was not correlated with the incidence of neuronal "background" discharges. Moreover, chronic exposure of serum-grown cultures to tetrodotoxin (TTX) in a dose sufficient to reversibly block bioelectric activity, failed to significantly affect this index. For explants grown in a chemically defined medium (CDM) similar excitability scores were obtained only if a low level of spontaneous activity was measured. The most active preparations scored considerably higher, with intermediate values being found in the moderately active cultures. Chronic TTX-exposure in developing CDM-grown cultures reduced their excitability scores to the level found in weakly active, untreated, explants despite a normal incidence of spontaneous activity. The present study indicates that low levels of spontaneous activity in untreated explants were associated with a similar sluggishness of DRG-evoked responses as previously observed after chronic treatment with TTX. These results give additional grounds for confidence that this reduced responsiveness of spinal cord neurons to sensory input is indeed attributable to prolonged reduction of centrally generated excitation during development in vitro.

Aging↗