Effect of Atropine on Histamine-Stimulated Gastric Secretion in the Dog

1956 ◽  
Vol 186 (3) ◽  
pp. 373-376 ◽  
Author(s):  
Henry D. Janowitz ◽  
Franklin Hollander
Keyword(s):  
Gastric Secretion ◽  
Parietal Cell ◽  
Acid Output ◽  
Inhibitory Effect ◽  
Atropine Sulphate ◽  
Secreting Cell ◽  
Secretory Rate ◽  
Acid Secreting ◽  
The Mean

Inhibitory effect of atropine on gastric acid secretion was studied in four dogs with vagally denervated corpus pouches, stimulated by 0.025 mg of histamine-base subcutaneous every 10 minutes. The mean inhibition of acid output in the 3rd hour after subcutaneous injection of atropine sulphate was 29% at 0.1 mg/kg body weight, 31% at 0.2 mg/kg, and 96% at 0.4 mg/kg. At the highest dosage, inhibition was virtually complete in six of seven experiments. Since current concepts of cholinergic blocking action by atropine on gastric secretion are not completely explanatory of the present results, possible alternative formulations of the role of acetylcholine and histamine in stimulating the parietal cell are presented. One of these postulates that histamine is the final common chemical pathway for all stimuli to the acid secreting cell. The existing evidence for this is reviewed briefly. In addition, further striking evidence is presented to support the hypothesis that the primary (parietal cell) acidity is relatively constant and independent of the secretory rate.

scholarly journals Demand on skillfulness modulates interhemispheric inhibition of motor cortices

2016 ◽  
Vol 115 (6) ◽  
pp. 2803-2813 ◽  
Author(s):  
Miles Wischnewski ◽  
Greg M. Kowalski ◽  
Farrah Rink ◽  
Samir R. Belagaje ◽  
Marc W. Haut ◽  
...  
Keyword(s):  
Primary Motor Cortex ◽  
Motor Task ◽  
Conditioning Stimulus ◽  
Motor Evoked Potential ◽  
Inhibitory Effect ◽  
Left Hand ◽  
The Mean ◽  
Small Targets ◽  
Healthy Participants

The role of primary motor cortex (M1) in the control of hand movements is still unclear. Functional magnetic resonance imaging (fMRI) studies of unimanual performance reported a relationship between level of precision of a motor task and additional ipsilateral M1 (iM1) activation. In the present study, we determined whether the demand on accuracy of a movement influences the magnitude of the inhibitory effect between primary motor cortices (IHI). We used transcranial magnetic stimulation (TMS) to measure active IHI (aIHI) of the iM1 on the contralateral M1 (cM1) in the premovement period of a left-hand motor task. Ten healthy participants manipulated a joystick to point to targets of two different sizes. For aIHI, the conditioning stimulus (CS) was applied to iM1, and the test stimulus (TS) to cM1, with an interstimulus interval of 10 ms. The amount of the inhibitory effect of the CS on the motor-evoked potential (MEP) of the subsequent TS was expressed as percentage of the mean MEP amplitude evoked by the single TS. Across different time points of aIHI measurements in the premovement period, there was a significant effect for target size on aIHI. Preparing to point to small targets was associated with weaker aIHI compared with pointing to large targets. The present findings suggest that, during the premovement period, aIHI from iM1 on cM1 is modulated by the demand on accuracy of the motor task. This is consistent with task fMRI findings showing bilateral M1 activation during high-precision movements but only unilateral M1 activity during low-precision movements.

Role of gastric acid secretion and blood flow in the development of vagal stimulation induced gastric mucosal damage

1993 ◽  
Vol 71 (10-11) ◽  
pp. 829-834 ◽  
Author(s):  
Lynn E. Hierlihy ◽  
John L. Wallace ◽  
Alastair V. Ferguson
Keyword(s):  
Blood Flow ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Vagal Stimulation ◽  
Mucosal Damage ◽  
Secretory Rate ◽  
The Mean ◽  
Gastric Mucosal Erosions

Vagal stimulation has been shown to result in the development of gastric mucosal erosions in the rat, although the mechanisms underlying the development of such erosions are not known. The effects of vagal stimulation on gastric acid secretion and mucosal blood flow were examined in urethane-anesthetized male Sprague–Dawley rats to determine whether changes in these factors correlate with the mucosal damage in response to vagal stimulation. Electrical stimulation (5 Hz, 5 V, 1 ms for 60 min) of afferent or efferent components of the vagi was not found to induce any significant increase in the mean acid secretory rate compared with control animals (p > 0.05). In contrast, stimulation of intact vagus nerves induced a significant increase in the mean acid secretory rate compared with control and efferent- and afferent-stimulated groups (p < 0.01). Measurement of gastric blood flow with laser-Doppler flowmetry demonstrated intact vagal stimulation to have no significant effect on gastric blood flow. These data suggest that such vagal stimulation induced increases in acid secretion in urethane-anesthetized animals may represent a part of the integrated physiological response to such stimulation which leads to the development of gastric mucosal erosions within 60 min. Pretreatment with antisecretory agents such as cimetidine and inter-leukin-1β significantly reduce the gastric mucosal injury compared with untreated animals (p < 0.05), emphasizing the important role of acid secretion in the development of vagal-induced gastric damage.Key words: vagus, acid secretion, blood flow, gastric.

Role of vagal and splanchnic capsaicin-sensitive afferents in enterogastric inhibition of acid secretion in rats

1995 ◽  
Vol 268 (2) ◽  
pp. G286-G291
Author(s):  
E. Saperas ◽  
J. Santos ◽  
J. R. Malagelada
Keyword(s):  
Acid Secretion ◽  
Acid Output ◽  
Inhibitory Effect ◽  
Intestinal Perfusion ◽  
Neural Pathways ◽  
Anesthetized Rats ◽  
Antisecretory Effect ◽  
Bilateral Vagotomy ◽  
Celiac Ganglionectomy

The role of capsaicin-sensitive afferent innervation and neural pathways involved in the enterogastric inhibition of gastric acid secretion by luminal acid was investigated in urethan-anesthetized rats. Intestinal perfusion with graded concentrations of HCl (50, 75, and 100 mM) for 1 h dose dependently inhibited both thyrotropin-releasing hormone (TRH) analogue- and pentagastrin-stimulated acid output (P < 0.01). The inhibitory effect of intestinal perfusion with HCl (100 mM) on pentagastrin-stimulated acid secretion was blocked by bilateral vagotomy, whereas celiac ganglionectomy had no effect. Systemic capsaicin pretreatment (125 mg/kg sc) reduced the antisecretory effects of luminal acid on both TRH analogue- and pentagastrin-stimulated acid secretion. Neither selective perivagal nor selective periceliac capsaicin treatments (1% solution) modified the antisecretory effect of intestinal perfusion with HCl (75 mM) on TRH analogue-stimulated acid secretion. However, combined selective perivagal plus periceliac capsaicin treatment reduced it to the same extent as systemic capsaicin treatment. We conclude that enterogastric inhibition of acid secretion by luminal acid in urethan-anesthetized rats is mediated by extrinsic reflexes involving both vagal and splanchnic capsaicin-sensitive afferent fibers.

Intracisternal TRH analogue RX 77368 stimulates gastric histamine release in rats

1990 ◽  
Vol 259 (4) ◽  
pp. G599-G604 ◽  
Author(s):  
K. Yanagisawa ◽  
Y. Tache
Keyword(s):  
Gastric Secretion ◽  
Interstitial Fluid ◽  
Acid Output ◽  
Histamine Secretion ◽  
Intracisternal Injection ◽  
Cervical Vagotomy ◽  
Hepatic Portal ◽  
The Brain ◽  
Related Increase

The influence of intracisternal injection of the stable thyrotropin-releasing hormone (TRH) analogue RX 77368 on histamine levels in gastric secretion, interstitial fluid of the fundic submucosa, and portal hepatic circulation was investigated in rats. Intracisternal injection of RX 77368 (10-300 ng) induced a dose-related increase in histamine and acid output measured in the gastric secretion of pylorus-ligated, conscious rats. Intracisternal RX 77368 (300 ng) induced within 20 min a significant twofold histamine increase in interstitial fluid sampled from dialysis fibers implanted into the fundic submucosa. Histamine levels in the hepatic portal circulation were also dose dependently increased by RX 77368 injected intracisternally (30-100 ng), whereas intravenous infusion of RX 77368 (300 ng/30 min) did not significantly modify portal histamine levels. Bilateral cervical vagotomy or atropine pretreatment prevented intracisternal RX 77368-induced rise in hepatic portal levels of histamine, whereas purified gastrin monoclonal antibody 9303, injected at a dose blocking gastrin-stimulated acid secretion, had no effect. These results indicate that RX 77368 acts in the brain to increase gastric histamine secretion through vagal-dependent, muscarinic, nongastrin-mediated mechanisms and suggest a possible role of medullary TRH in the vagal regulation of gastric histamine secretion.

Renin secretory effects of N6-cyclohexyladenosine: effects of dietary sodium

1987 ◽  
Vol 252 (5) ◽  
pp. F872-F876 ◽  
Author(s):  
P. C. Churchill ◽  
N. F. Rossi ◽  
M. C. Churchill
Keyword(s):  
Adenosine Receptors ◽  
Inhibitory Effect ◽  
Renin Secretion ◽  
Dietary Sodium ◽  
Secretory Rate ◽  
Renal Cortical Slice ◽  
The Mean ◽  
Induced Changes ◽  
Cortical Slices

Previous observations by others have shown that Na deprivation augments and Na loading attenuates the inhibitory effect of exogenous adenosine on renin secretion in vivo. The purpose of the present experiments was to test the hypothesis that Na deprivation and Na loading alter the sensitivity of the adenosine receptors (A1 subclass) that mediate the inhibitory effect. The rat renal cortical slice preparation was used. Na loading decreased and Na deprivation increased tissue renin content and the basal renin secretory rate; these two variables were directly related (r = 0.84, P less than 0.00005). N6-cyclohexyladenosine (CHA), an adenosine analogue that selectively activates the A1 subclass of adenosine receptors in the nanomolar to micromolar concentration range inhibited renin secretion over the same range of concentrations (nM-microM) and to approximately the same maximal extent (to 50% of the mean basal secretory rate) in cortical slices taken from Na-loaded, control, and Na-deprived rats. These results demonstrate that changes in the intrinsic sensitivity of adenosine receptors do not explain dietary Na-induced changes in the in vivo renin secretory response to exogenous adenosine.

Vagotomy confined to the acid-secreting mucosa of the stomach

1987 ◽  
Vol 73 (1) ◽  
pp. 25-30
Author(s):  
E. P. Dewar ◽  
N. S. Williams ◽  
M. F. Dixon ◽  
D. Johnston
Keyword(s):  
Gastric Secretion ◽  
Myenteric Plexus ◽  
Acid Output ◽  
Gastric Wall ◽  
Neural Tissue ◽  
Gastric Fistula ◽  
Gastric Acid Output ◽  
Before And After ◽  
Acid Secreting ◽  
Gastric Musculature

AbstractChemoneurolysis, using varying concentrations of ethyl alcohol, was performed in dogs with a total gastric fistula in an attempt to denervate selectively only the acid-secreting mucosa, leaving the muscle innervated. Tests of gastric secretion and histological examination of gastric wall biopsies were performed both before and after chemoneurolysis. Chemoneurolysis resulted in a significant reduction in the number of parasympathetic fibres in the submucosa (p<0.01) and a decrease in insulin and pentagastrin stimulated acid secretion. The appearances of the myenteric plexus and gastric musculature were unchanged. The destruction of the submucosal neural tissue was, however, insufficient to produce a th erapeutically significant decrease in gastric acid output.

Effect of total adrenalectomy on gastric secretion in chronic gastric fistula rats

1964 ◽  
Vol 206 (6) ◽  
pp. 1309-1314 ◽  
Author(s):  
S. P. Bralow ◽  
S. A. Komarov ◽  
H. Shay
Keyword(s):  
Gastric Secretion ◽  
Parietal Cell ◽  
Free Acid ◽  
Acid Output ◽  
Cell Mass ◽  
Chloride Concentration ◽  
Sham Operation ◽  
Gastric Fistula ◽  
Total Acid ◽  
Total Chloride

Basal gastric secretion of rats with chronic fistulas was studied before and after adrenalectomy or sham operation. A marked exponential fall in concentration and output of free and total acid resulted in virtual anacidity within 3–7 weeks following adrenalectomy. Failure in parietal cell secretion was not accompanied by significant decrease in parietal cell mass. Pepsin concentration and output as well as volume also fell exponentially but more gradually. No significant change in total chloride concentration occurred. Relative influence of concentration in determining output was 30 times greater than volume for free acid, 3 times greater for total acid, and twice as great for pepsin. Volume was responsible for almost all variability in total chloride output. Time after adrenalectomy influenced variability of volume and acid output twice as much as concurrent decrease in body weight.

Effect of sodium pentobarbital on histamine stimulated gastric secretion

1961 ◽  
Vol 201 (3) ◽  
pp. 574-576 ◽  
Author(s):  
A. P. Skyring ◽  
G. W. Milton ◽  
G. A. Maxwell
Keyword(s):  
Gastric Secretion ◽  
Direct Effect ◽  
Intravenous Injection ◽  
Parietal Cell ◽  
Inhibitory Effect ◽  
Significant Inhibition ◽  
Sodium Pentobarbital ◽  
Depth Of Anesthesia ◽  
Heidenhain Pouch ◽  
Dose Levels

The inhibitory effect of sodium pentobarbital on histamine stimulated gastric secretion was studied in Heidenhain pouch dogs. An intravenous injection of sodium pentobarbital in a dose of 26 mg/kg produced significant inhibition of secretion at dose levels of histamine from 5.5 µg/histamine base/kg/10 min to 22 µg/histamine base/kg/10 min. The degree of inhibition produced was inversely proportional to the dose of histamine used but was not dependent on the depth of anesthesia. It is concluded that this effect is probably a direct effect on the parietal cell.

Basal and pentagastrin-stimulated gastric secretion in young horses

1990 ◽  
Vol 259 (6) ◽  
pp. R1259-R1266
Author(s):  
M. L. Campbell-Thompson ◽  
A. M. Merritt
Keyword(s):  
Gastric Secretion ◽  
Acid Concentration ◽  
Acid Output ◽  
Sodium Concentration ◽  
Gastric Fluid ◽  
Ion Concentration ◽  
Hydrogen Ion Concentration ◽  
Secretory Rate ◽  
Young Horses ◽  
Marked Drop

Equine gastric secretion was studied using a gastric cannula model after fasting (basal) and pentagastrin infusion. Gastric secretory rate, pH, osmolality, and electrolyte concentrations and outputs were determined over a 5-h period. Dose-response tests estimated that the maximally effective intravenous dose of pentagastrin was between 3 and 6 micrograms.kg-1.h-1. Basal secretory rate was 278 +/- 29 (SE) ml/15 min, and the pH was 2.00 +/- 0.31. Pentagastrin infusion at 6 micrograms.kg-1.h-1 increased secretory rate to 533 +/- 60 ml/15 min and decreased pH to 1.41 +/- 0.11. Basal gastric acid concentration and output were 38 +/- 5 meq/l and 211 +/- 36 mu eg.kg-1.h-1, respectively. Pentagastrin increased acid concentration to 60 +/- 5 meq/l and acid output to 474 +/- 61 mu eq.kg-1.h-1. Gastric fluid osmolality remained hypotonic during both basal and pentagastrin conditions. Sodium concentration remained high in comparison with hydrogen ion concentration, and sodium output increased during pentagastrin infusion. Equine gastric secretion did not attain maximal acid concentrations nor the marked drop in pH, which has been reported for other monogastric species. These data suggest that in the horse a large nonparietal component exists that modifies parietal secretions and is increased by pentagastrin stimulation.

Mechanism of action of insulin hypoglycemia on gastric secretion in man

1960 ◽  
Vol 15 (4) ◽  
pp. 697-703 ◽  
Author(s):  
David C. H. Sun ◽  
Harry Shay
Keyword(s):  
Gastric Secretion ◽  
Mechanism Of Action ◽  
Adrenal Glands ◽  
Acid Output ◽  
Late Phase ◽  
Inhibitory Effect ◽  
Maximal Response ◽  
Insulin Hypoglycemia ◽  
Before And After ◽  
Total Adrenalectomy

The effect of insulin hypoglycemia on acid output of gastric secretion over 5-hour periods was studied in eighteen patients with duodenal ulcer, five patients before and after vagotomy and two patients before and after bilateral total adrenalectomy. Results of this study show three components of the mechanism of action of insulin hypoglycemia on gastric secretion, an initial inhibitory effect on basal gastric secretion, a stimulating effect mediated through the vagus nerve responsible for the early phase of secretion (1st and 2nd hr.) and. a gastric secretory response mediated through the adrenal glands manifested in the late phase of secretion (3rd–5th hr.). However, the magnitude of this late phase of gastric secretion was considerably less pronounced after vagotomy. It appears that a maximal response of this phase of gastric secretion following insulin hypoglycemia dependent on the adrenal gland is also dependent upon an intact vagal mechanism. A significant hypoglycemia of 40 mg % or less was necessary to produce the late phase of gastric secretion. The adrenal phase can contribute to the potential for ulcer occurrence or reactivation, not so much through the increase in secretion it alone might induce, since this is small, but of greater importance in its synergistic action with the vagal mechanism. Submitted on December 9, 1959

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