scholarly journals Inhibition of Gastric Acid Secretion by Unfractionated and Low Molecular Weight Heparins in the Rat

2006 ◽  
Vol 6 ◽  
pp. 221-230
Author(s):  
Omar M.E. Abdel Salam ◽  
Ayman R. Baiuomy ◽  
Amany Ameen
Keyword(s):  
Molecular Weight ◽  
Risk Factor ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Intraperitoneal Administration ◽  
Low Molecular Weight ◽  
Gastric Erosions ◽  
Low Molecular Weight Heparins

The majority of patients receiving heparin preparations are at stress, which is a risk factor for the development of gastric erosions. Our aim was to examine the effect of unfractionated heparin (UFH) and low molecular weight heparins (LMWHs) on gastric acid secretion. Gastric acid secretion was induced in urethane-anesthetized rats by distention of the stomach (2 ml saline for 2 h) in addition to histamine or bethanechol stimulation. Distension-stimulated acid secretion (2 ml for 2 h) was significantly inhibited by intraperitoneal administration of UFH (2000 IU/kg, 19% reduction), enoxaparin (180 or 360 IU/kg, 59.2 and 87.1%, reduction, respectively), nadroparin (1000 or 2000 IU/kg, 36 and 60.7% reduction, respectively), and tinzaparin (3000 IU/kg, 41.3% reduction). All tested heparins also suppressed acid secretion in response to distention and histamine or bethanechol stimulation. Pretreatment with indomethacin did not abolish the gastric inhibitory action of nadroparin. After truncal vagotomy or atropine, nadroparin failed to inhibit acid secretion stimulated by histamine. Ganglionic blockade with guanethidine abolished the gastric inhibitory action of nadroparin or UFH. It is concluded that both UFH and LMWHs administered peripherally inhibit stimulated gastric acid secretion in the rat. This effect of heparins is determined by cholinergic and partly by adrenergic mechanisms.

Role of gastric acid secretion in progression of acute gastric erosions induced by ischemia–reperfusion into gastric ulcers

2000 ◽  
Vol 398 (1) ◽  
pp. 147-158 ◽  
Author(s):  
Tomasz Brzozowski ◽  
Peter Ch Konturek ◽  
Stanislaw J Konturek ◽  
Danuta Drozdowicz ◽  
Slawomir Kwiecieñ ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Ischemia Reperfusion ◽  
Gastric Ulcers ◽  
Gastric Erosions

scholarly journals The mechanism of inhibitory action of secretin on gastric acid secretion in conscious rats.

1995 ◽  
Vol 488 (2) ◽  
pp. 501-508 ◽  
Author(s):  
K Shimizu ◽  
P Li ◽  
K Y Lee ◽  
T M Chang ◽  
W Y Chey
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Conscious Rats

scholarly journals Central Site of Inhibitory Action of Bombesin on Gastric Acid Secretion in Rats

1987 ◽  
Vol 45 (2) ◽  
pp. 129-133
Author(s):  
Yasunobu OKUMA ◽  
Kunihiko YOKOTANI ◽  
Yoshitsugu OSUMI
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action

scholarly journals Central site of inhibitory action of bombesin on gastric acid secretion in rats.

1987 ◽  
Vol 45 (2) ◽  
pp. 129-133 ◽  
Author(s):  
Yasunobu OKUMA ◽  
Kunihiko YOKOTANI ◽  
Yoshitsugu OSUMI
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action

Helicobacter pylori infection is a major risk factor in the decrease of gastric acid secretion in the elderly

2000 ◽  
Vol 118 (4) ◽  
pp. A1306
Author(s):  
Tomohiko Shimatani ◽  
Masaki Inoue ◽  
Yoko Horikawa ◽  
Yukinobu Kawai ◽  
Nobue Harada ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Risk Factor ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
The Elderly ◽  
Helicobacter Pylori Infection ◽  
Major Risk Factor

scholarly journals Inhibitory action of E3810, a new H+-K+ ATPase inhibitor, on H+-K+ ATPase anil gastric acid secretion in vitro

1989 ◽  
Vol 49 ◽  
pp. 196
Author(s):  
Hideaki Fujisaki ◽  
Kiyoshi Oketani ◽  
Hisashi Shibata ◽  
Manabu Murakami ◽  
Tsuneo Wakabayashi ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Atpase Inhibitor

CRF initiates biological actions within the brain that are observed in response to stress

1987 ◽  
Vol 252 (1) ◽  
pp. R34-R39 ◽  
Author(s):  
H. J. Lenz ◽  
A. Raedler ◽  
H. Greten ◽  
M. R. Brown
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Plasma Catecholamine ◽  
Biological Actions

Corticotropin-releasing factor (CRF) is thought to be an endogenous mediator of adrenocorticotropic hormone release following stress. We examined if CRF initiates further biological actions that are observed in response to stressful events. Male beagle dogs (10–12 kg) were fitted with a chronic intracerebroventricular cannula, intra-arterial and intravenous catheters, as well as a gastric fistula. Synthetic human CRF was microinjected into the third cerebral ventricle in conscious animals. CRF (0.1–1.0 nmol/kg) significantly (P less than 0.01) increased plasma concentrations of epinephrine, norepinephrine, glucagon, and glucose and elevated mean arterial pressure and heart rate. Pretreatment of the animals with the ganglionic blocking agent chlorisondamine completely abolished the increases in plasma catecholamine and glucose concentrations as well as the elevations in blood pressure and heart rate. CRF significantly (P less than 0.01) inhibited gastric acid secretion, but not plasma gastrin concentrations stimulated by an 8% liquid peptone meal. The gastric inhibitory action of CRF was completely prevented by chlorisondamine and, in part, by naloxone and a vasopressin antagonist. In contrast, bilateral truncal vagotomy did not affect the gastric inhibitory action of CRF. The results of this study indicate that CRF acts within the central nervous system to increase plasma glucose and glucagon concentrations, mean arterial pressure, and heart rate by activation of the autonomic nervous system. CRF inhibits meal-stimulated gastric acid secretion by activation of the sympathetic nervous system and, in part, by opiate and vasopressin-dependent pathways and not by inhibition of gastrin release.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathways mediating CRF-induced inhibition of gastric acid secretion in rats

1989 ◽  
Vol 256 (1) ◽  
pp. G214-G219 ◽  
Author(s):  
G. Druge ◽  
A. Raedler ◽  
H. Greten ◽  
H. J. Lenz
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Plasma Concentrations ◽  
Conscious Rats ◽  
The Central Nervous System

The pathways involved in mediating the central nervous system actions of corticotropin-releasing factor (CRF) on gastric acid secretion were examined in conscious rats. CRF (0.1-2.0 nmol) given cerebroventricularly inhibited gastric acid secretion stimulated by pentagastrin (P less than 0.01). This effect was abolished by cerebroventricular but not intravenous administration of a specific CRF receptor antagonist, alpha-helical CRF-(9-41). Ganglionic blockade with chlorisondamine chloride, noradrenergic blockade with bretylium, or adrenalectomy abolished the gastric inhibitory action of CRF whereas truncal vagotomy or opiate blockade with naloxone did not. A vasopressin receptor antagonist significantly inhibited but did not abolish the gastric inhibitory action of CRF. An intravenous infusion of epinephrine that mimicked the epinephrine plasma concentrations which were observed after cerebroventricular administration of CRF did not alter pentagastrin-stimulated gastric acid secretion. These results indicate that CRF acts within the central nervous system to inhibit gastric acid secretion by a specific receptor-mediated event. Inhibition of gastric acid secretion by CRF in conscious rats is mediated by efferent fibers of the sympathetic nervous system and in part by a vasopressin-dependent pathway but not by the parasympathetic nervous system, adrenal epinephrine release, or opiate-sensitive pathways.

Apolipoprotein A-IV acts in the brain to inhibit gastric emptying in the rat

1996 ◽  
Vol 270 (1) ◽  
pp. G49-G53 ◽  
Author(s):  
T. Okumura ◽  
K. Fukagawa ◽  
P. Tso ◽  
I. L. Taylor ◽  
T. N. Pappas
Keyword(s):  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Intraperitoneal Administration ◽  
Phenol Red ◽  
Dependent Manner ◽  
Liquid Meal ◽  
Apolipoprotein A ◽  
Intracisternal Injection

We have very recently shown that intracisternal injection of apolipoprotein A-IV (apo A-IV), a glycoprotein produced in the small intestine by fat, dose-dependently inhibited gastric acid secretion in pylorus-ligated conscious rats. These results suggest that apo A-IV acts centrally as a neuromodulator to inhibit gastric secretion. The present study was carried out to examine the hypothesis that apo A-IV acts centrally to alter gastric emptying. Rats fasted 24 h received intracisternal injection of apo A-IV and a liquid meal by oral intubation under brief isoflurane anesthesia. Gastric emptying of a liquid meal was determined by the phenol red method. Intracisternal injection of apo A-IV inhibited gastric emptying of a liquid meal in a dose-dependent manner (1.0-4.0 micrograms). On the other hand, apo A-I in a dose of 4 micrograms failed to change gastric emptying. Gastric emptying was not altered by intraperitoneal administration of apo A-IV in a dose of 15 micrograms. These results suggest that apo A-IV acts centrally to delay gastric emptying of a liquid meal. Together with our recent finding that apo A-IV acts centrally to inhibit gastric acid secretion, the present study supports our hypothesis that apo A-IV may be involved in lipid-induced inhibition of gastric function.

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