Electrical stimulation of the vagus nerve modulates the histamine content of mast cells in the rat jejunal mucosa

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

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 ◽  
...  

1990 ◽  
Vol 68 (6) ◽  
pp. 2305-2311 ◽  
Author(s):  
J. N. Baraniuk ◽  
M. L. Kowalski ◽  
M. A. Kaliner

Electrical stimulation of rat sensory nerves produces cutaneous vasodilation and plasma protein extravasation, a phenomenon termed “neurogenic inflammation”. Rat skin on the dorsum of the paw developed neurogenic inflammation after electrical stimulation of the saphenous nerve. In tissue sections, the extravasation of the supravital dye monastral blue B identified permeable vessels. Mast cells were identified by toluidine blue stain. Permeable vessels were significantly more dense in the superficial 120 microns of the dermis than in the deeper dermis, whereas mast cells were significantly more frequent in the deeper dermis. The relationships between nociceptive sensory nerve fibers, permeable vessels, and mast cells were examined by indirect immunohistochemistry for calcitonin gene-related peptide (CGRP), neurokinin A (NKA), and substance P (SP). CGRP-, NKA-, and SP-containing nerves densely innervated the superficial dermis and appeared to innervate the vessels that became permeable during neurogenic inflammation. In contrast, mast cells were not associated with either permeable vessels or nerve fibers. These data suggest that electrical stimulation of rat sensory nerves produces vascular permeability by inducing the release of neuropeptides that may directly stimulate the superficial vascular bed. Mast cells may not be involved in this stage of cutaneous neurogenic inflammation in rat skin.


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