• Biomolecules & Therapeutics
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• v.7 no.2
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• pp.105-111
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• 1999

Nitric oxide (NO), a cellular messenger synthesized from L-arginine by NO synthase (NOS, EC.1.14.13.39), is considered to be a regulator of gastric secretion. In the present study, the role of NO in the regulation of exocrine secretion was investigated in rat gastric chief cells. Treatment of chief cells with carba-chol resulted in an increase in the arginine conversion to citrulline, the amount of $NO_{x}$, the release of pepsine-gen, and the level of cGMP Especially, carbachol-stimulated increase of arginine to citrulline transformation, the amount of $NO_{x}$, cGMP level and the release of pepsinogen were partially reduced by the natural NOS inhibitor, $N^{G}$-monomethyl-L-arginine (MMA) and $N^{G}$, $N^{G}$-dimethyl-L-arginine (DMA). Furthermore, MMA- and DMA-induced decrease of pepsinogen secretion showed dose-dependent patters. Activation of NOS is one of the early events in receptor-mediated cascade of reactions in gastric chief cells and NO, not completely, but partially mediates gastric secretion. Agonist-stimulated pepsinogen secretion in chief cells has been considered to be mediated in adenosine 3',5'-cyclic monophosphate pathway and/or guanosine 3', 5'-cyclic monophosphate (cGMP) pathway. Taken together, the above results suggest that partial decrease of exocrine secretion following treatment of NOS inhibitor may result from the inactivation of NOS and subsequent guano- late cyclase, and NO/cGMP pathway may play a pivotal role in exocrine secretion.

• Korean Journal of Pharmacognosy
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• v.15 no.3
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• pp.128-133
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• 1984

The extracts of Yukgunja-tang which has been used in some of gastroin testinal disorders were examined for secretion of gastric juice and movement of isolated stomach of rabbit. Experiments were performed with the dried extract of Yukgunja-tang (sample I) and the dried extract compound made of each drug of Yukgunja-tang (sample II). The secretion of gastric juice at the doses of 25.0 and 50.0mg/kg p.o. of sample I showed the decreases of 34.3 and 43.3%, respectively, as compared with control group, whereas the secretion at a dose of 76.8g/kg of sample II showed 43.1%. In gastric acid secretion, sample I showed 50.0% decrease at a dose of 50.0mg/kg and sample II showed 46.2% decrease at a dose of 76.8mg/kg. In pepsin output sample I showed 17.8 and 23.4% decreases at a dose of 25.0 and 50.0mg/kg, respectively, whereas sample II showed 22.5% decrease at a dose of 76.8mg/kg. The isolated stomach of rabbit showed dose-responsive contraction by addition of sample I, however the contraction was not observed by sample II.

• Biomolecules & Therapeutics
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• v.4 no.1
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• pp.84-88
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• 1996

Alnus japonica cortex has been used as antidiarrhea, antihemorrhage and the remedy of indigestion. This study was performed to investigate the effectiveness of the methanol extracts of the Alnus japonica cortex on the gastric lesion and ulcer. The methanol extract was fractionated with hexane, chloroform and butanol, followed by bioassay on antigastritic and antiulcer activity. The methanol extract showed low acute toxicity with minimum lethal dose of more than 5000 mg/kg, p.o. in mice. The chloroform and the butanol fraction reduced gastric lesion in HCI. ethanol induced gastritic model. On gastric secretion in pylorus ligated rat, the hexane and chloroform fraction decreased the volume and acidity. The butanol fraction had significant inhibitory effects on aspirin and Shay's ulcer. The butanol fraction showed a tendency to inhibit the decrease of mucin secretion due to ingestion of absolute ethanol.

• YAKHAK HOEJI
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• v.36 no.2
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• pp.173-179
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• 1992

The rhizoma of Zingiber officinale has been used as antiemetic, expectorants, stomachache relieving drugs and digestive accelerators. From the observation of antigastritic action of the methanol extract of the rhizoma, it was fractionated with hexane, chloroform, ethyl acetate and butanol, followed by bioassay on antigastritic and antiulcerative activity. The hexane and the chloroform fraction reduced significantly HCl ethanol induced gastric lesion at the dose of 370 and 210 mg/kg, p.o., respectively. On the gastric ulceration and gastric secretion in pylorus-ligated rats, the hexane fraction decreased the volume of gastric secretion and acid output, and also increased pH at the dose of 370 mg/kg, i.d.. It showed considerable curative ratio of acetic acid induced ulcer without inhibition of indomethacin induced gastric lesion. The methanol extract showed low acute toxicity with minimum lethal dose of more than 3000 mg/kg, p.o. in mice. In conclusion, Zingiberis rhizoma exhibited antigastric and antiulcerative activity which might be attributable to inhibition of gastric secretion. It is revealed that the active component may be present in the hexane fraction.

• Journal of Food Hygiene and Safety
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• v.14 no.4
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• pp.358-364
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• 1999

Propolis, a natural resinous compound collected from honey bees, contains many biochemical constituents and has been used in traditional medicines as early as 300 B.C. Recently, it has been reported to possess many biological activities such as antibacterial, antiviral, fungicidal, local anaesthetic, immunostimulating, antiinflammatory and free radical scavenging properties. This study was performed to investigate the pharmacological effects of the propolis extract and fractions on the gastric lesion and ulcer. The ethanol extract was fractionated with hexane, toluene and ethyl acetate. Followed by bioassay on antigastric and antiulcer activity. Propolis ethanol extracts(500, 750, 1,000, 1,500 and 2,000 mg/kg) showed the protective effect on HCl·ethanol-induced gastric lesion and the antisecretory effect against Shay’s gastric secretion in pylorus-ligated rats in a dose related manner. In the animal models of HCl·ethanol, aspirin-induced gastric lesion and Shay’s gastric secretion, the hexane and toluene fraction of propolis significantly reduced the length of gastric lesion and the acid secretion. These data showed that the gastric protective effects of propolis might result from reduction of acid secretion through the inactivation of H+/K+ATPase activity.

• The Korean Journal of Physiology
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• v.23 no.2
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• pp.393-399
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• 1989

Sixty-seven conscious rats prepared with chronic gastric fistula were studied to examine the effect of vagotomy on gastric secretory responses to medial amygdaloid stimulation. Gastric acid output was significantly increased by electrical stimulation of the medial amygdaloid nucleus, and the increases in acid secretion were completely eliminated by vagotomy. However, in rats subjected to stimulation of the medial amygdaloid nucleus plus vagotomy, acid output was almost same as that in only vagotomized rats. And vagotomy itself decreased the acid secretion significantly. These results indicate that the influence of electrical stimulaton of the medial amygdaloid nucleus on acid secretion is carried largely via vagus nerves. And also, without electrical stimulation of medial amygdaloid nucleus, acid secretion is controlled by way of vagus in rats. Plasma gastrin concentrations were measured following stimulation of the medial amygdaloid nucleus. Plasma levels of gastrin were not significantly altered by stimulation of the medial amygdaloid nucleus with or without vagotomy. It is therefore inferred from the above results that the facilitatory influence of the medial amygdaloid nucleus on the gastric acid secretion is mediated chiefly via vagal activity and that gastrin is not responsible for the increase in acid secretion in this process.

• The Korean Journal of Physiology
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• v.18 no.2
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• pp.117-124
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• 1984

It has been recently reported that cingulate cortex mar facilitate gastric acid secretion, but its facilitatory mechanism on the gastric acid secretion is still unclear. This study was undertaken to investigate the facilitatory mechanism of the cingulate cortex upon gastric acid secretion in rats. Twenty·three male albino rats were divided into the cingulate(N= 13) and the operated control(N= 10) groups. The cingulate group in which cingulate cortex was removed by suction through a slit-shaped opening on each side of, and parallel to, the sagittal suture. In the operated control group, the surgical procedure was ended with the skull opening and the incision of dura mater. The gastric juice was collected via a chronic gastric cannula after 24 hours of fast, with water ad libitum. The juice was collected continuously for 6 hours, starting 3 hours prior to the injection of gastric secretagogue, pentagastrin$(12\;{\mu}g/kg)$ or histamine dihydrochloride $(320\;{\mu}g/kg)$. Three one·hour samples were obtained before ana after the administration of each secretagogue. The two agents were injected separately and subcutaneously at intervals of 1 week, the blood samples were drawn from the abdominal aorta for the radioimmunoassay of postprandial plasma gastrin concentration in response to the forced feeding of 10% cod liver oil. 1) After pentagastrin administration, the volume of gastric juice tended to decrease, but its acidity tended to increase in the cingulate group compared with those of the operated control group. However, there was no any difference in the acid output between the two groups. 2) Histamine-stimulated acid output and volume of the gastric juice of the cingulate group decreased significantly compared with those of the operated control group, while there was not significantly different in the acidity between the two groups. 3) Before pentagastrin or histamine administration, any change was not observed in the gastric acid secretion following the cingulate cortical ablation. 4) Postprandial plasma gastrin concentration in response to the forced feeding of 10% cod liver oil was insignificantly lower in the cingulate group than in the operated control group. It is inferred from the above results that the cingulate cortex exerts a facilitatory influence upon the histamine-stimulated gastric acid secretion in rats, and its influence may not be mediated by the stimulation of gastrin secretion.

• YAKHAK HOEJI
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• v.40 no.4
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• pp.456-461
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• 1996

The effects of human epidermal growth factor(EGF) which was produced by recombinant DNA technique was investigated on gastric secretion, gastric lesion and ulcer models in rats. The EGF showed significant inhibition of secretion of gastric juice and total acid output, at 0.4mg/kg, id and also inhibited Shay ulceration at 0.4mg/kg, id in rats. The lesion induced by absolute ethanol was significantly reduced by oral administration of EGF at 0.4mg/kg. Likewise, EGF caused significant inhibition of indomethacin induced gastric ulcer at oral doses of 0.2 and 0.4mg/kg. The EGF produced dose-dependent inhibition of gastric ulcer induced by acidified aspirin, but showed no significant inhibition at oral doses of 0.1, 0.2 and 0.4mg/kg. The chronic gastric ulcer induced by injection of 20% acetic acid solution was significantly reduced by oral doses of 0.1 and 0.4mg/kg of EGF. Duodenal ulcer induced by mepirizole was dose-dependently inhibited by oral doses of 0.1, 0.2 and 0.4mg/kg of EGF. These data suggest that EGF possesses pronounced inhibitory action in gastric ulcer and duodenal ulcer of rats.

• The Korean Journal of Physiology
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• v.22 no.2
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• pp.179-187
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• 1988

This study was conducted to investigate the effects of epinephrine and norepinephrine on basal gastric acid secretion and plasma gastrin and secretin concentration in the conscious rat. One hundred and eighty-four albino rats with gastric cannula were used after 18 hours or more of fast, with water ad libitum. In a restraint cage for collection of gastric juice, physiological saline (0.9% NaCl) was continuously infused into the jugular vein through a catheter for one hour at a rate of 1 ml/hr (control period). Immediately after the control period, epinephrine (1, 2, 4, 8 and $16{\mu}g/ml/hr)$, norepinephrine (1, 2, 4, 8 and $16{\mu}g/ml/hr)$ or physiological saline (1 ml/hr) was infused for another one hour. Gastric juice was collected at one hour interval for two hours infusion period. Adrenergic antagonists, phentolamine and propranolol were injected into the jugular vein 5 min prior to the infusion of epinephrine or norepinephrine at a dose of 0.2 mg/0.1 ml. Blood was sampled from the jugular vein for the radioimmunoassay of plasma gastrin and secretin after the collection of gastric juice. The results were as follows: 1) Both epinephrine and norephinephrine significantly increased gastric acid output in a dosedependent manner. 2) The effects of epinephrine and norepinephrine on the gastric acid secretion were antagonized by the pretreatment with phentolamine and propranolol. 3) Plasma gastrin and secretin concentrations were not significantly affected by the intravenous infusion of epinephrine and norepinephrine. It can be inferred from the above results that epinephrine and norepinephrine facilitate gastric acid secretion in conscious rats and the mechanism of which is attributed to ${\alpha}\;and\;{\beta}$ adrenergic receptors rather than gastrin and secretin.

• The Korean Journal of Physiology
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• v.23 no.1
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• pp.119-127
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• 1989

This study was undertaken to investigate the effect of medial amygdala on the gastric acid secretion and plasma gastrin concentration in the rats with chronic gastric fistula. After the medial nucleus of amygdala was damaged bilaterally by radiofrequency a. c. through stereotaxically inserted electrodes, the gastric juice was collected in the basal and histamine-stimulated states for 1 hour. The gastric juice was also collected while the medial nucleus of amygdala was stimulated with biphasic square wave in the both states. After the collection of the gastric juice, blood samples were drawn from the abdominal aorta for the radioimmunoassay of plasma gastrin. The results were as follows: 1) The damage of the medial amygdala significantly decreased the gastric juice volume and the acid output in the histamine-stimulated state. 2) The electrical stimulation of the medial amygdala significantly increased the gastric juice volume and the acid output in the histamine-stimulated state, and the acid output in the basal state. 3) The damage of the medial amygdala significantly decreased the plasma gastrin concentration but the electrical stimulation of the medial amygdala did not affect the plasma gastrin concentration. It is therefore suggested that the medial amygdala has a facilitatory influence on the histamine-stimulated gastric acid secretion in rats, and the influence may not be attributed to gastrin release.