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.

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.

Autonomic pathways in development of neural stimulation-induced gastric mucosal damage

1994 ◽  
Vol 266 (2) ◽  
pp. G179-G185 ◽  
Author(s):  
L. E. Hierlihy ◽  
J. L. Wallace ◽  
A. V. Ferguson
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Vagal Stimulation ◽  
Gastric Damage ◽  
Gastric Mucosal Damage ◽  
Cervical Cord ◽  
Sprague Dawley ◽  
Vagus Nerves ◽  
Surgical Interventions ◽  
Autonomic Nervous

Gastric mucosal erosions can be induced by electrical stimulation of either vagus nerves (5 Hz, 5 V, 1 ms) or the paraventricular nucleus (PVN) of the hypothalamus (200 microA, 60 Hz, 100-microseconds pulse width). We have utilized various pharmacological and surgical interventions to determine the contributions of different components of the autonomic nervous system to the development of this neurally induced gastric damage in urethan-anesthetized Sprague-Dawley rats. In all experiments damage was assessed macroscopically and scored blindly on a 0 (normal) to 3 (severe) scale with samples sectioned for subsequent histological assessment of damage at the light microscopic level. Animals pretreated with either hexamethonium (30 mg/kg iv) or atropine (2 mg/kg iv) demonstrated reduced gastric damage scores after vagal stimulation compared with untreated control animals (P < 0.05). In contrast animals that underwent cervical cord transection exhibited gastric damage after both vagal and PVN stimulation that was not significantly different compared with animals with an intact cord undergoing similar stimulation (P > 0.05). Such cord transection itself did not cause any significant change to the gastric mucosa in the time period studied. These data emphasize the importance of the autonomic nervous system, in particular the parasympathetic component in the development of vagal stimulation-induced gastric damage. In addition, the present studies suggest that neither vagal nor PVN stimulation-induced gastric damage is dependent on neural projections to sympathetic preganglionic neurons of the intermediolateral cell column of the spinal cord.

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.

scholarly journals The Gastroprotective Effect of Vitex pubescens Leaf Extract against Ethanol-Provoked Gastric Mucosal Damage in Sprague-Dawley Rats

PLoS ONE ◽  
2016 ◽  
Vol 11 (9) ◽  
pp. e0157431 ◽  
Author(s):  
Nahla Saeed AL-Wajeeh ◽  
Mohammed Farouq Halabi ◽  
Maryam Hajrezaie ◽  
Summaya M. Dhiyaaldeen ◽  
Daleya Abdulaziz Bardi ◽  
...  
Keyword(s):  
Leaf Extract ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Sprague Dawley ◽  
Gastroprotective Effect ◽  
Sprague Dawley Rats

scholarly journals Correction: The Gastroprotective Effect of Vitex pubescens Leaf Extract against Ethanol-Provoked Gastric Mucosal Damage in Sprague-Dawley Rats

PLoS ONE ◽  
2017 ◽  
Vol 12 (5) ◽  
pp. e0179072
Author(s):  
Nahla Saeed AL-Wajeeh ◽  
Mohammed Farouq Halabi ◽  
Maryam Hajrezaie ◽  
Summaya M. Dhiyaaldeen ◽  
Daleya Abdulaziz Bardi ◽  
...  
Keyword(s):  
Leaf Extract ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Sprague Dawley ◽  
Gastroprotective Effect ◽  
Sprague Dawley Rats

scholarly journals Effects of polaprezinc on gastric mucosal damage and neurotransmitters in a rat model of chemotherapy-induced vomiting

2018 ◽  
Vol 46 (6) ◽  
pp. 2436-2444
Author(s):  
Zhao Yang Liu ◽  
Wen Bo Xie ◽  
Ming Ru Li ◽  
Nan Teng ◽  
Xiao Liang ◽  
...  
Keyword(s):  
Rat Model ◽  
Mucosal Injury ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Control Group ◽  
Sprague Dawley ◽  
Serum Samples ◽  
Sprague Dawley Rats ◽  
Hematoxylin And Eosin ◽  
Brain Tissues

Objective To investigate the effects of polaprezinc (PZ) on cyclophosphamide (CTX)- or cisplatin (DDP)-induced gastric mucosal injury and on a rat model of neurotransmitter-mediated vomiting. Methods Sprague–Dawley rats were divided at random into Control, CTX, DDP, PZ+CTX, and PZ+DDP groups. After 20 days, brain tissues and sera were analyzed for the levels of dopamine (DA), 5-hydroxytryptamine (5-HT), and nuclear factor kappa B (NF-κB). Hematoxylin and eosin-stained sections of stomach, intestine, and brain tissues were examined using light microscopy. Results The levels of DA, 5-HT, and NF-κB in brain and serum samples of rats treated with CTX or DDP were significantly increased compared with those of rats in the Control group. There was a significant decrease in these values in the PZ group. Moreover, PZ reduced damage to brain tissue caused by CTX or DDP. Conclusions PZ decreased the levels of DA, 5-HT, and NF-κB in blood and brain tissues caused by CTX or DDP and reduced the chemotherapy-induced damage to the small intestine, stomach, and brain. These findings can be translated to the clinic to enhance the efficacy and safety of chemotherapy.

Vagal feedback with expiratory threshold load under extracorporeal circulation

1983 ◽  
Vol 55 (2) ◽  
pp. 316-322 ◽  
Author(s):  
Y. Jammes ◽  
P. T. Bye ◽  
R. L. Pardy ◽  
C. Roussos
Keyword(s):  
Extracorporeal Circulation ◽  
Vagal Stimulation ◽  
Inhibitory Response ◽  
Vagal Afferents ◽  
Vagus Nerves ◽  
Anesthetized Dogs ◽  
Expiratory Muscles ◽  
Evoked Activity ◽  
Proprioceptive Inputs ◽  
Stimulation Of

In 11 anesthetized dogs placed under extracorporeal circulation, the vagal feedback was tested by electrical stimulation of the vagus nerves with cold block of their caudal part and by passive lung hyperinflation. The apneic response to such vagal stimulation progressively disappeared during expiratory threshold load breathing but then returned to control values some minutes after the load was removed. This suppression of the inhibitory response to stimulation of the vagus nerves was usually observed when vagal afferents were intact or blocked by cold. However, it was not observed whether no evoked activity continued in expiratory muscles after the cold block, or after suppression of all proprioceptive muscular afferents after transection of the spinal cord at C6 level. These results strongly suggest that enhancement of proprioceptive inputs to the respiratory centers counteracts the vagally mediated inspiratory “off-switch” mechanisms.

Endogenous CCK disrupts the MMC pattern via capsaicin-sensitive vagal afferent fibers in the rat

1997 ◽  
Vol 272 (1) ◽  
pp. G100-G105 ◽  
Author(s):  
A. Rodriguez-Membrilla ◽  
P. Vergara
Keyword(s):  
Intravenous Infusion ◽  
Sprague Dawley ◽  
Rat Intestine ◽  
Intracerebroventricular Infusion ◽  
C Fibers ◽  
Afferent Fibers ◽  
Sprague Dawley Rats ◽  
Vagal Afferent ◽  
Endogenous Release ◽  
Stimulation Of

A meal disrupts migrating motor complexes (MMC) in the rat intestine through stimulation of peripheral cholecystokinin (CCK)-B and central CCK-A receptors. The aim of this study was to determine pathways implicated in postprandial disruption of the MMC mediated by CCK. Sprague-Dawley rats were prepared with electrodes for electromyography in the small intestine, and ablation of vagal afferent C-fibers by capsaicin was carried out. Endogenous release of CCK was induced by oral administration of soybean trypsin inhibitor (SBTI). In control rats SBTI disrupted MMC and generated an irregular spiking activity that lasted longer than 3 h. Intravenous infusion of L-365,260 (2 x 10(-7) mol/kg) but not of L-364,718 (3 x 10(-9) mol/kg) restored the MMC pattern. In capsaicin-treated rats, SBTI did not modify fasting activity. Infusion of CCK octapeptide (CCK-8) at 3 x 10(-9) mol.kg-1.h-1 disrupted the MMC, although the response was quantitatively and qualitatively different from SBTI. The effect was reversed by intravenous infusion of L-364,718 or L-365,260 and intracerebroventricular infusion of L-364,718. In capsaicin-treated rats, the intracerebroventricular or intravenous infusion of L-364,718 inhibited CCK-8 effects. However, the intravenous infusion of L-365,260 did not reverse the MMC pattern. These results suggest that the disruption of the MMC mediated by CCK is due to stimulation of peripheral CCK-B receptors located in vagal afferent fibers. This initiates a reflex including stimulation of central CCK-A receptors. Exogenous CCK also stimulates peripheral CCK-A receptors not located in capsaicin-sensitive vagal afferent fibers.

scholarly journals Contrasting pharmacological ETB receptor blockade with genetic ETB deficiency in renal responses to big ET-1

2001 ◽  
Vol 6 (1) ◽  
pp. 39-43 ◽  
Author(s):  
DAVID M. POLLOCK
Keyword(s):  
Renal Plasma Flow ◽  
Urine Flow ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Clearance Studies ◽  
Etb Receptor ◽  
Pharmacological Blockade ◽  
Series Of Experiments ◽  
Renal Responses

Renal clearance studies were conducted to determine the role of ETB receptors in the renal response to big endothelin-1 (big ET-1). Two series of experiments were conducted on Inactin-anesthetized rats to contrast acute pharmacological blockade of ETB receptors vs. genetic ETB receptor deficiency. In the first series, Sprague-Dawley rats were given either ETB-selective antagonist, A-192621, or vehicle (0.9% NaCl) prior to infusion of big ET-1 (10 pmol·kg−1·min−1) for 60 min. A-192621 significantly increased baseline mean arterial pressure (MAP; 102 ± 4 vs. 141 ± 6 mmHg, P < 0.05) and urine flow rate (0.5 ± 0.1 vs. 1.3 ± 0.2 μl/min, P < 0.05) without any effect on glomerular filtration rate (GFR) or effective renal plasma flow (ERPF). Big ET-1 significantly increased MAP in both groups but to a higher level in rats given antagonist (120 ± 6 vs. 169 ± 6 mmHg, P < 0.05). Big ET-1 increased urine flow in control rats but decreased in rats given antagonist. GFR and ERPF were decreased in rats given big ET-1, an effect that was exaggerated by ETB blockade. Another series of experiments examined the response to big ET-1 in rats lacking functional renal ETB receptors, known as spotting lethal ( sl) rats. Surprisingly, rats heterozygous ( sl/+) for ETB receptor deficiency had a significantly higher baseline MAP compared with homozygous ( sl/ sl) rats (134 ± 6 vs. 112 ± 7 mmHg, P < 0.05), although other variables were similar. Big ET-1 produced no significant change in MAP in either group. Urine flow, GFR, and ERPF were significantly decreased in both groups, although these changes were much larger in sl/ sl rats. These experiments indicate that the ETB receptor plays an important role in limiting the renal hemodynamic response to big ET-1. Furthermore, the diuretic actions of big ET-1 require a functional ETB receptor.

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