New technique for vagal nerve stimulation

Goldberger, Jeffrey J.; Kadish, Alan H.; Johnson, David C.; Qi, Xiaoshi

doi:10.1016/s0165-0270(99)00085-0

Cited by 9 publications

(8 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Parasympathetic effects on cardiac electrophysiology have been studied by nerve stimulation or pharmacological blockade in resting conditions (13,22,30,32). Parasympathetic activation prolongs sinus cycle length, AV conduction time, and ventricular refractory period.…”

Section: Discussionmentioning

confidence: 99%

Parasympathetic effects on cardiac electrophysiology during exercise and recovery

Kannankeril

Goldberger

2002

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Depressed parasympathetic tone is associated with an increased risk of sudden cardiac death. Exercise and the postexercise recovery period, which are associated with parasympathetic withdrawal, are high risk periods for sudden death. However, parasympathetic effects on cardiac electrophysiology during exercise and recovery have not been described. Electrophysiology studies were performed using noninvasive programmed stimulation (NIPS) in nine subjects (age 59 Ϯ 18 yr) with implanted dual-chamber devices and normal left ventricular function during multiple bicycle exercise sessions. NIPS was performed at rest, during exercise, and in the early recovery period both before and after parasympathetic blockade with atropine. Parasympathetic effect was defined as the value of the parameter of interest in the absence of atropine minus the value of the parameter in the presence of atropine. During exercise, sinus cycle length, atrioventricular (AV) block cycle length, AV interval, and ventricular effective refractory period shortened; in recovery, the values were intermediate between the rest and exercise values (P Ͻ 0.0001 by ANOVA). Parasympathetic effects on sinus cycle length, AV block cycle length, AV interval, and ventricular effective refractory period were 247 Ϯ 140, 58 Ϯ 20, 76 Ϯ 20, and 8.6 Ϯ 7.5 ms at rest, 106 Ϯ 20, 37 Ϯ 14, 24 Ϯ 13, and 2.6 Ϯ 7.8 ms during exercise, and 209 Ϯ 114, 50 Ϯ 23, 35 Ϯ 21, and 9.5 Ϯ 11.8 ms during recovery, respectively. There was poor correlation among the parasympathetic effects noted at the sinus node, AV node, and ventricle. Further work evaluating parasympathetic effects on cardiac electrophysiology during exercise and recovery in patients with heart disease is required to elucidate its role in modulating the risk of sudden cardiac death noted at these times. exercise THE RISK OF SUDDEN DEATH is increased nearly 17-fold during and immediately after exercise (2, 23). While there are several potential mechanisms for this marked increased risk of sudden cardiac death, it is possibly related in part to the acute changes in autonomic tone that accompany exercise. Exercise is associated with increased sympathetic tone and parasympathetic withdrawal in normal subjects (11,12,36).Numerous clinical and experimental studies have provided evidence linking diminished parasympathetic nervous system activity at rest with increased mortality and sudden cardiac death (6,16,18,28,31). Experimental data suggest that dogs with myocardial infarctions prone to ventricular fibrillation during exercise and induced ischemia have greater reductions in parasympathetic tone, as measured by heart rate variability, during exercise compared with nonsusceptible animals (7). Recent human data have shown that a small heart rate decrease in the early recovery phase after exercise is associated with an increased mortality (9,10,27). These data suggest that depressed parasympathetic tone during exercise or depressed recovery of parasympathetic tone after exercise may be important factors resulting in an increased...

show abstract

Section: Discussionmentioning

confidence: 99%

Parasympathetic effects on cardiac electrophysiology during exercise and recovery

Kannankeril

Goldberger

2002

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…An attractive hypothesis is that parasympathetically induced changes in cardiac electrophysiology exert antiarrhythmic effects. It is well known that parasympathetic stimulation affects sinus nodal automaticity and AV nodal dromotropy (94,95). Several studies have also demonstrated changes in ventricular refractoriness with parasympathetic stimulation or blockade (96,97); parasympathetic effects on ventricular refractoriness may be antiarrhythmic.…”

Section: Issues For Further Studymentioning

confidence: 99%

Assessment of Autonomic Function in Cardiovascular Disease

Lahiri

Kannankeril

Goldberger

2008

Journal of the American College of Cardiology

477

382

View full text Add to dashboard Cite

Certain abnormalities of autonomic function in the setting of structural cardiovascular disease have been associated with an adverse prognosis. Various markers of autonomic activity have received increased attention as methods for identifying patients at risk for sudden death. Both the sympathetic and the parasympathetic limbs can be characterized by tonic levels of activity, which are modulated by, and respond reflexively to, physiological changes. Heart rate provides an index of the net effects of autonomic tone on the sinus node, and carries prognostic significance. Heart rate variability, though related to heart rate, assesses modulation of autonomic control of heart rate and carries additional prognostic information, which in some cases is more powerful than heart rate alone. Heart rate recovery after exercise represents the changes in autonomic tone that occur immediately after cessation of exercise. This index has also been shown to have prognostic significance. Autonomic evaluation during exercise and recovery may be important prognostically, because these are high-risk periods for sudden death, and the autonomic changes that occur with exercise could modulate this high risk. These markers provide related, but not redundant information about different aspects of autonomic effects on the sinus node.

show abstract

“…The vagus nerve participates in the regulation of pancreatic juice secretion. Several studies have shown that electrical vagal stimulations induced the release of CCK-8 into the circulation [ 22 , 23 , 46 ]. Our study demonstrated that the vagal stimulation increased the volume and the protein and trypsin outputs in pancreatic juice.…”

Section: Discussionmentioning

confidence: 99%

“…The involvement of vagal nerves was examined following subdiaphragmatic vagotomy and capsaicin deafferentation, as described previously [ 20 , 21 ]. The Neuropack (Nihon Kohden Co., Tokyo, Japan) apparatus was used to stimulate the vagus nerve (rate, 1 Hz; duration, 0.2 ms; V-range, 2 mV; stim., 4.2 mA) [ 22 , 23 ].…”

Section: Methodsmentioning

confidence: 99%

Effect of Adropin on Pancreas Exocrine Function in a Rat Model: A Preliminary Study

Kapica

Puzio

Abramowicz

et al. 2022

Animals

View full text Add to dashboard Cite

The aim was to investigate the potential effect of adropin (ADR) on pancreatic–biliary juice (PBJ) secretion (volume, protein content, trypsin activity) in a rat model. The animals were divided into control and five experimental groups: adropin, CCK-8 (CCK-8 stimulation), capsaicin (capsaicin deactivation of afferents), vagotomy (vagotomy procedure), and vagal stimulation (vagal nerve stimulation). The experiment consisted of four phases, during which vehicle (0.9% NaCl) and three ADR boluses (5, 10, and 20 µg/kg BW) were administered i.v. every 30 min. PBJ samples were collected from each rat at 15 min intervals after boluses. Exogenous ADR failed to affect the pancreatic responses after vagotomy and the capsaicin pretreatment and reduced the PBJ volume, protein outputs, and trypsin activity in the adropin, CCK-8, and vagal stimulation groups in a dose-dependent manner. In all these groups, volume of PBJ was reduced only by the highest dose of ADR (p < 0.001 for adropin group and p < 0.01 for CCK-8 and vagal stimulation groups), and the protein outputs were reduced by the administration of ADR 10 µg/kg BW (adropin and CCK-8 groups, p < 0.01 in both cases) and 20 µg/kg BW (p < 0.001 for adropin and CCK-8 groups, p < 0.01 for vagal stimulation group). The 10 µg/kg BW dose of ADR reduced the trypsin output in the CCK-8 group (p < 0.01), and the highest ADR dose reduced the trypsin output in the CCK-8 (p < 0.001) and vagal stimulation (p < 0.01) groups. In conclusion, adropin in the analyzed doses exhibits the negative feedback pathway. This mechanism seems to participate in the regulation of pancreatic juice secretion via an indirect vagal mechanism.

show abstract

New technique for vagal nerve stimulation

Cited by 9 publications

References 13 publications

Parasympathetic effects on cardiac electrophysiology during exercise and recovery

Parasympathetic effects on cardiac electrophysiology during exercise and recovery

Assessment of Autonomic Function in Cardiovascular Disease

Effect of Adropin on Pancreas Exocrine Function in a Rat Model: A Preliminary Study

Contact Info

Product

Resources

About