Neurally mediated gastric mucosal damage in hypophysectomized rats

1992 ◽  
Vol 70 (8) ◽  
pp. 1109-1116 ◽  
Author(s):  
Lynn E. Hierlihy ◽  
John L. Wallace ◽  
Alastair V. Ferguson
Keyword(s):  
Electrical Stimulation ◽  
Paraventricular Nucleus ◽  
Mucosal Damage ◽  
Pituitary Hormones ◽  
Gastric Damage ◽  
Gastric Mucosal Damage ◽  
Sprague Dawley ◽  
Vagal Nerves ◽  
Scale Control ◽  
Stimulation Of

The role of the pituitary hormones in the development of neurally mediated gastric mucosal damage was examined in both normal and hypophysectomized urethane-anaesthetized male Sprague–Dawley rats. Gastric mucosal damage was elicited either by electrical stimulation of intact vagal nerves or by electrical stimulation in the paraventricular nucleus. Macroscopic damage was scored following the stimulation period and samples of the stomach were fixed for histological assessment. Damage scores were assigned based on a 0 (normal) to 3 (severe) scale. Control experiments in which the vagi were not stimulated did not result in any significant gastric damage in either normal (0.56) or sham surgery (0.14) animals, whereas hypophysectomized animals were observed to have significant damage (1.44, p < 0.05). Stimulation of the vagi in hypophysectomized animals resulted in damage that was not significantly different compared with the hypophysectomized control animals (1.25, p > 0.05). In normal animals, stimulation of vagal nerves resulted in mean damage scores of 2.00, values that were not significantly different from those observed in hypophysectomized animals (1.25, p > 0.05). Similarly, stimulation in the paraventricular nucleus of hypophysectomized animals resulted in gastric lesions (2.00) that were not significantly different from those observed in normal animals (1.91, p > 0.05). These data suggest that such neurally mediated gastric damage does not depend upon neurosecretory projections to the pituitary gland, but that the maintenance of an intact gastric mucosa under normal conditions requires the presence of pituitary hormones.Key words: vagus, paraventricular nucleus, hypophysectomy, gastric.

Vagal stimulation-induced gastric damage in rats

1991 ◽  
Vol 261 (1) ◽  
pp. G104-G110
Author(s):  
L. E. Hierlihy ◽  
J. L. Wallace ◽  
A. V. Ferguson
Keyword(s):  
Vagal Stimulation ◽  
Mucosal Damage ◽  
Vagal Afferents ◽  
Gastric Damage ◽  
Gastric Mucosal Damage ◽  
Sprague Dawley ◽  
Vagus Nerves ◽  
Sprague Dawley Rats ◽  
Series Of Experiments ◽  
Stimulation Of

The role of the vagus nerve in the development of gastric mucosal damage was examined in urethan-anesthetized male Sprague-Dawley rats. Electrical stimulation was applied to the vagus nerves for a period of 60 min, after which macroscopic gastric damage was scored and samples of the stomach were fixed for later histological assessment. Damage scores were assigned blindly based on a 0 (normal) to 3 (severe) scale. Stimulation of vagal afferents or efferents in isolation did not result in significant damage to the gastric mucosa (P greater than 0.1). In contrast, stimulation of both intact vagus nerves resulted in significant gastric mucosal damage (mean damage score, 2.0 +/- 0.33, P less than 0.01). A second series of experiments demonstrated this gastric damage to be induced within 30-60 min; extending the stimulation period to 120 min did not worsen the gastric damage scores significantly (P greater than 0.1). In a third study, stimulation of both intact vagus nerves after paraventricular nucleus (PVN) lesion resulted in damage scores (0.33 +/- 0.17) that were significantly reduced compared with intact PVN and non-PVN-lesioned animals (P less than 0.01). These results indicate that the development of vagal stimulation-induced gastric damage requires the activation of both afferent and efferent vagal components and suggest further that such damage is dependent upon an intact PVN.

Leptin acts in the rat hypothalamic paraventricular nucleus to induce gastric mucosal damage

1998 ◽  
Vol 275 (6) ◽  
pp. R2081-R2084
Author(s):  
Pauline M. Smith ◽  
Veronique Mollaret ◽  
Alastair V. Ferguson
Keyword(s):  
Paraventricular Nucleus ◽  
Area Under Curve ◽  
Mucosal Damage ◽  
System Structure ◽  
Gastric Mucosal Damage ◽  
Sprague Dawley ◽  
Specific Population ◽  
Regulate Body Weight ◽  
Sprague Dawley Rats ◽  
A Site

Leptin is produced and secreted by adipocytes to regulate body weight homeostasis. Leptin acts centrally to reduce weight by decreasing food intake and increasing energy expenditure. The paraventricular nucleus (PVN) is a central nervous system structure suggested as a site at which leptin acts to exert its central effects. Leptin microinjection (10−6 M, 0.5 μl) into the PVN of urethan-anesthetized male Sprague-Dawley rats (150–300 g) resulted in significant gastric damage (mean score = 1.75, n = 16). Damage scores were significantly different than those observed after saline microinjection into the PVN (mean score = 0.00, n = 5, P < 0.05), or leptin microinjection into non-PVN sites (mean score = 0.33, n = 6, P < 0.05). There were no changes in blood pressure (mean area under curve = 401.9 ± 224.2 mmHg * s, n = 11, P > 0.05) or heart rate (mean area under curve = 40.9 ± 25.9 beats, n= 10, P > 0.05) in response to leptin microinjection into PVN. These results suggest that leptin acts on a functionally specific population of PVN neurons involved in the control of gastrointestinal function.

Hypothalamic projections of renal afferent nerves in the cat

1980 ◽  
Vol 58 (5) ◽  
pp. 574-576 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Fluid Balance ◽  
Lateral Hypothalamus ◽  
Discharge Rate ◽  
Renal Nerves ◽  
Preoptic Nucleus ◽  
Afferent Nerves ◽  
Stimulation Of

In 10 cats anaesthetized with chloralose the electrical activity of spontaneously active hypothalamic units was recorded for changes in discharge rate during electrical stimulation of renal afferent nerves. The discharge rate of 141 single units was altered by stimulation of either the ipsilateral or contralateral renal nerves. Most of the responsive units were located in the regions of lateral preoptic nucleus, lateral hypothalamus, and paraventricular nucleus. These results demonstrate that renal afferent nerves provide information to hypothalamic structures known to be involved in the regulation of arterial pressure and fluid balance.

scholarly journals Utility of Periurethral Electric Stimulation to Reduce Voiding Frequency in Rats

2009 ◽  
Vol 3 (2) ◽  
Author(s):  
A. Forrest ◽  
Y. Zhang ◽  
A. Bicek ◽  
G. Timm
Keyword(s):  
Electrical Stimulation ◽  
Electric Stimulation ◽  
The United States ◽  
The Body ◽  
Bladder Pressure ◽  
Urinary Continence ◽  
Sprague Dawley ◽  
Promising Alternative ◽  
Surgical Interventions ◽  
Stimulation Of

Urinary continence is maintained through coordination of electrical (nervous) and mechanical (muscles, ligaments and other structures) systems in the body. During micturition, the central nervous system sends a signal to the detrusor and sphincter muscles to coordinate voiding. Pathological problems can undermine either of the two systems and result in urinary incontinence (UI). Thirteen million people in the United States live with UI. Clinical treatments to date are largely mechanical in nature, restoring function through surgical interventions. However, electrically-based treatments, such as electric stimulation, offer a promising alternative. Here we investigate the utility of electrical stimulation of the periurethral neuromusculature to reduce voiding contractions in well-controlled animal experiments. Female Sprague Dawley rats were anesthetized with a ketamine/xylazine/acepromazine cocktail and the bladder was catheterized through a small incision in the bladder dome and was infused with saline. Continuous filling of the bladder triggered related cycles of voiding which was identified through bladder pressure increases and visual urination. The pubic symphysis bone was cut to expose the urethra and a stimulating electrode was placed in the periurethral region. The electrical stimulation parameters were 2.8 mA of current, 200 us pluses, and 20 Hz. The electrical stimulation was done in fifteen minute intervals. Statistically, the rats without electrical stimulation have an average contraction period of 63.1 sec (+/– 31.3 sec) and the rats with electrical stimulation have an average contraction period of 97.2 sec (+/– 43.0 sec). The results showed that the electrical stimulation of the periurethral neuromusculature in the group revealed 54.0% increase in average contraction period and decrease in voiding frequency. Electrical stimulation of the periurethral neuromusculature increases the voiding interval and void volume for the rats. This suggests the existence of an external urinary sphincter to the bladder inhibitory pathway and supports periurethral neuromusculature stimulation as an alternative to spinal nerve stimulation for the treatment of bladder overactivity.

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