scholarly journals Avoiding off-target effects in electrical stimulation of the cervical vagus nerve: Neuroanatomical tracing techniques to study fascicular anatomy of the vagus nerve

2019 ◽  
Vol 325 ◽  
pp. 108325 ◽  
Author(s):  
Nicole Thompson ◽  
Svetlana Mastitskaya ◽  
David Holder
2017 ◽  
Vol 47 (3) ◽  
pp. 345-351
Author(s):  
S. Yu. Zhilyaev ◽  
A. N. Moskvin ◽  
T. F. Platonova ◽  
I. T. Demchenko

1983 ◽  
Vol 244 (4) ◽  
pp. E317-E322 ◽  
Author(s):  
F. Rohner-Jeanrenaud ◽  
A. C. Hochstrasser ◽  
B. Jeanrenaud

In vivo glucose-induced insulin secretion was greater in preweaned preobese 17-day-old Zucker rats than in the corresponding controls. This hypersecretion of insulin was reversed to normal by acute pretreatment with atropine. A short-lived (30 s) electrical stimulation of the vagus nerve preceding a glucose load potentiated the in vivo glucose-induced insulin release in adult animals (6-9 wk) and more so in obese Zucker (fa/fa) than in lean rats. This suggested the existence of enhanced sensitivity and/or responsiveness of the B cells of obese animals to the parasympathetic system. That the parasympathetic tone was increased in adult obese Zucker (fa/fa) rats was corroborated by the observation that acute vagotomy of these animals resulted in a significant decrease in glucose-induced insulin secretion, whereas no such effect was seen in lean rats. Also, perfused pancreases from adult obese (fa/fa) rats oversecreted insulin during a stimulation by arginine when compared with controls, an oversecretion that was restored toward normal by superimposed infusion of atropine. It is concluded that a) the increased insulin secretion of preobese Zucker fa/fa rats is an early abnormality that is mediated by the vagus nerve, and b) increased secretion of insulin in adult obese fa/fa rats continues to be partly vagus-nerve mediated, although a decreased sympathetic tone and other unknown defects could conceivably play a role as well.


2019 ◽  
Vol 97 (8) ◽  
pp. 766-772
Author(s):  
Ezidin G. Kaddumi

The coexistence of different visceral pathologies in patients suffering from irritable bowel syndrome, interstitial cystitis, and other pathologies, necessitates the study of these pathologies under complicated conditions. In the present study, cystometry recordings were used to investigate the effect of distal esophageal chemical irritation on the urinary bladder interaction with distal colon distention, distal esophageal distention, and electrical stimulation of abdominal branches of vagus nerve. Distal esophageal chemical irritation significantly decreased the intercontraction time via decreasing the voiding time. Also, distal esophageal chemical irritation significantly decreased the pressure amplitude by decreasing the maximum pressure. Following distal esophageal chemical irritation, distal esophageal distention was able to significantly decrease the intercontraction time by decreasing the storage time. However, 3 mL distal colon distention significantly increased the intercontraction time by increasing the storage time. On the other hand, following distal esophageal chemical irritation, electrical stimulation of abdominal branches of vagus nerve did not have any significant effect on intercontraction time. However, electrical stimulation of abdominal branches of vagus nerve significantly increased the pressure amplitude by increasing the maximum pressure. The results of this study demonstrate that urinary bladder function and interaction of bladder with other viscera can be affected by chemical irritation of distal esophagus.


2012 ◽  
Vol 61 (2) ◽  
pp. 156-165 ◽  
Author(s):  
Magdalena Szczerbowska-Boruchowska ◽  
Anna Krygowska-Wajs ◽  
Agata Ziomber ◽  
Piotr Thor ◽  
Pawel Wrobel ◽  
...  

Neuroreport ◽  
1995 ◽  
Vol 7 (1) ◽  
pp. 313-317 ◽  
Author(s):  
Thomas P. Gottwald ◽  
Bryan R. Hewlett ◽  
Sárka Lhoták ◽  
Ron H. Stead

1990 ◽  
Vol 68 (10) ◽  
pp. 1363-1367 ◽  
Author(s):  
Don W. Wallick ◽  
Sherry L. Stuesse ◽  
Paul Martin

A brief electrical stimulation of the vagus nerve may elicit a triphasic response comprising (i) an initial prolongation of the same or the next cardiac cycle, (ii) a return of the subsequent cardiac cycle to about the level prior to vagal stimulation, and (iii) a secondary prolongation of cardiac cycle length that lasts several beats. We compared the effects of two calcium channel antagonists, verapamil and nifedipine, on this triphasic response to vagal stimulation in chloralose-anesthetized, open-chest dogs. In the absence of vagal stimulation, nifedipine (doses of 10, 40, and 50 μg/kg for a total dose of 100 μg/kg, i.v.) and verapamil (two doses of 100 μg/kg each, i.v.) increased the cardiac cycle length (A–A interval) by 16% (429 ± 20 to 496 ± 21 ms) and 29% (470 ± 33 to 605 ± 54 ms), respectively. Nifedipine (100 μg/kg total) attenuated the initial vagally mediated prolongation of the A–A interval, from 474 ± 19 to 369 ± 42 ms above the basal A–A interval. Following the initial prolongation of the vagal effect, other A–A intervals were not affected. In contrast, verapamil potentiated the vagally mediated initial prolongation in cardiac cycle length at the first dose administered (100 μg/kg) from 492 ± 17 to 561 ± 14 ms, but other increases in dosages had no further effect. Thus these two calcium channel antagonists have different effects on the sinoatrial chronotropic responses caused by brief vagal stimulation.Key words: autonomic control, parasympathetic, heart, calcium.


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