• The Korean Journal of Physiology
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• 제23권1호
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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.

• Journal of Digestive Cancer Research
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• 제10권1호
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• pp.9-15
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• 2022

Proton pump inhibitors (PPIs), a potent gastric acid inhibitor, are widely used in gastric acid-related diseases such as gastroesophageal reflux disease and peptic ulcer, and are known as the most frequently used drugs worldwide. However, as the frequency of use increases, the number of cases of long-term PPI therapy without clear indications is increasing. Recently, there have been concerns about the risk of gastric cancer in patients with long-term PPI users. Potential mechanisms for the association between PPI and gastric cancer include enterochromaffin-like cell proliferation due to hypergastrinemia caused by gastric acid suppression, progression of atrophic gastritis, and corpus-predominant type through interaction with Helicobacter pylori (H. pylori) infection. Several epidemiologic studies showed controversial results on the issue, and it is difficult to prove a causal relationship between PPI and gastric cancer. Nevertheless, long-term PPI should be administered cautiously based on individual risk-benefit profile, specifically among those with history of H. pylori infection, in high-risk region of gastric cancer.

• 한국미생물·생명공학회지
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• 제31권3호
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• pp.297-300
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• 2003

In order to select probiotics with a high survival rate in gut and the growth inhibition of virulent pathogens to human beings or animals, we have screened lactic acid bacteria and yeasts from Jeot-gal to assess resistance against the artificial gastric acid and bile juice. Lactic acid bacteria and yeasts isolated were incubated for 24 h in artificial bile juice after incubation for 2 h in artificial gastric acid. Especially, strain HW 161 and strain NK 181 showed the higher survival for 2 h incubation in artificial gastric acid. All of 3 strains of lactic acid bacteria and 2 strains of yeast were showed higher growth rate than the control in artificial bile. The antimicrobial activity of lactic acid bacteria and yeasts was also investigated to prove efficacy as probiotic organisms. Lactic acid bacteria were shown the inhibition of Gram positive and negative bacteria, but yeasts narrow inhibition.

• 대한약리학회지
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• 제17권1호
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• pp.27-32
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• 1981

It has been known that ethanol stimulates the secretion of gastric acid regardless of its route of administration. Recently, however, some studies have challenged this view and claimed that ethanol inhibits the gastric acid secretion. This study was undertaken to investigate the effects of ethanol on the gastric acid secretion in anesthetized rat in respect to the route of administration and the concentration of alcohol. Normal saline (pH adjusted to 6.0) was used as standard perfusion solution and ethanol was mixed as 0.8, 1.7, 5, 10 and 20%. Four ml of perfusion fluid was given into stomach via gastric tube and drained from duodenal tube every 5 min. Acid secretion was measured by back titration to pH 6.0 with N/20 NaOH and expressed as ${\mu}Eq/5$ min. Low concentration of ethanol up to 1.7% in perfusion solution caused little changes in acid secretion, but moderate concentration such as perfusion of 5% or 10% ethanol solution inhibited both the basal and histamine-induced gastric secretion. Moreover, loss of perfused acid was seen by 20% ethanol, which means back diffusion of hydrogen ions into the gastric mucosa. However, intravenous administration of ethanol, maintained at the level of 0.1% alcohol in blood, caused significant stimulation of gastric acid. We, therefore, conclude that in anesthetized rat ethanol has dual effects on acid secretion, i.e., inhibiting and enhancing by oral and intravenous administration, respectively, but further investigation is necessary to clarify these effects.

• 대한약리학회지
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• 제31권1호
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• pp.75-84
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• 1995

NO의 위산분비에 대한 작용을 규명하기 위하여 분리한 토끼위선세포에서 hypoxia/reoxygenation과 acidosis후 위산분비와 NO synthase 활성을 측정하였다. 분리한 위선세포에 30분의 hypoxia와 1시간의 reoxygenation을 주었으며, acidosis를 위하여 배지의 pH를 6.0과 4.0으로 변화시켜 실험하였다. 위산분비는 위선세포 내와 외의 $[^{14}C]-aminopyrine$ 축적비율로 측정하였으며, NO synthase 활성은 NO의 전구물질인 $[^{14}C]L-arginine$으로부터 $[^{14}C]-citrulline$으로의 전환율로 결정하였다. 결과로서 dibutyryl cAMP는 농도 의존적으로 위산분비를 촉진시켰으나 NO synthase 활성엔 영향을 주지 않았다. Hypoxia/reoxygenation은 기초 및 자극 위산분비를 억제하였으며 acidosis에 의해 위산분비억제는 더욱 심화되었다. Constitutive NO synthase 활성 역시 hypoxia/reoxygenation과 acidosis에 의해 억제되었다. 결론적으로 hypoxia/reoxygenation과 acidosis 같은 위점막의 병적상태는 위산분비와 NO 유리를 모두 억제하나, 기초상태의 위선에서 dibutyryl cAMP에 의한 위산분비 촉진에 대한 NO의 직접적인 작용은 확인되지 않았다.

• The Korean Journal of Physiology
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• 제22권2호
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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.

• 대한기관식도과학회지
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• 제1권1호
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• pp.55-63
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• 1995

Gastroesophageal reflux is thought to be an important etiology of the various upper aerodigestive tract disease. To investigate the role of gastric acid and pepsin as an etiologic factor of laryngotracheal stenosis, and the difference of injury by synthetic gastric juice between in ciliated respiratory epithelium and in squamous epithelium, experimental study was carried out using rabbits. Mucociliary transport affected by synthetic gastric juice was also studied in dogs. Synthetic gastric juice of low pH caused serious damage and Impairment of mucociliary transport in the epithelium of the larynx and trachea. Gastric acid played major role in the mucosal damage. Squamous epithelium of vocal folds and pharynx was more resistant to synthetic gastric juice than respiratory epitheium. In conclusion, gastroesophageal reflux may be an etiologic factor in the developement of laryngotracheal stenosis, so the adequate management is necessory In patients of laryngotracheal stenosis.

• Archives of Pharmacal Research
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• 제25권1호
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• pp.61-66
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• 2002

From our previous result that Panax ginseng head extract had inhibition of gastric damages, the extract was fractionated. Among the hexane, chloroform, butanol and water fractions, butanol fraction Showed the most potent inhibition of HCl.ethanol-induced gastric lesion, aspirin-induced gastric ulcer, acetic acid-induced ulcer and Shay ulcer. Butanol fraction showed significant increase in mucin secretion, and inhibited malondialdehyde (MDA) and $H^{+}/K^{+}ATPase$ activity in the stomach. This results indicate that the effectiveness of the fraction on gastric damages might be related to inhibition of acid secretion, increment of mucin secretion and antioxidant property.

• Biomolecules & Therapeutics
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• 제3권1호
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• pp.72-79
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• 1995

The antiulcer effects of newly synthesized prostaglandin derivatives were investigated in various experimental ulcer models and on gastric secretion in rats. HK-3 and HK-4, PG $E_2$derivatives, prevented the formation of acute gastric ulcer induced by ethanol or aspirin in pylorus-ligated rats. The ulcer formation was moderately inhibited by HK-1 and HK-2, PG $F_{2{\alpha}}$ derivatives, and aggravated by SK-1, SK-2 and SK-3, PG $F_{2{\alpha}}$ derivatives. HK-3 and HK-4 reduced the volume, acid output and pepsin output of gastric juice in pylorus-ligated rats. The gastric perfusion with physiologic saline(pH 6.0) showed relatively constant acid secretion and indomethacin increased the acid secretion. The acid secretion was markedly decreased by PG $E_2$but PG $F_{2{\alpha}}$ caused little change. Prostaglandin derivatives, especially HK-3 arid HK-4, significantly inhibited the acid secretion induced by indomethacin. The results show that, PG $E_2$ derivatives, HK-3 and HK-4, inhibit acid secretion and also have protective effects on gastric ulceration induced by ethanol or aspirin.

• 동의생리병리학회지
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• 제24권6호
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• pp.970-975
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• 2010

Because Lonicerae Flos has effects of antiinflammatory and antioxidant, we studied an effect of Lonicerae Flos on reflux esophagitis (RE) through those effects. Rats were treated with three different dosages of LF (500, 250 and 125 mg/kg) orally for 14 days before pylorus and forestomach ligation. Six hrs after pylorus and forestomach ligation, we dissected a stomach and examined a stomach volume, gastric acid output, pepsin release in the stomach, total hexose, sialic acid in stomach tissue and histamine contents of sera. The results were compared with an ${\alpha}$-tocopherol (once orally, 1hr before operation, 30 mg/kg) treated group in which the effects on RE were already confirmed. Lonicerae Flos extract (LE) reduced gastric volumes compared to RE control. This indicate that LE protect a stomach mucosa by depressing of gastric acid release and corresponse with a reducing histamine content of serum. And LE decreasd a volume of pepsin in stomach compraed to RE control, LE increased contents of total hexose and sialic acid based on esophageal and gastric mucus. This indicated that an increased mucus by LE protected inflammation of esophagus mucosa and gastric mucosa induced by gastric acid. So, LE suppressed a gasric acid by decreasing a pepsin release in stomach, suppressed an injury of esophagus inducted by gastric acid with increasing esophageal mucus and a minimum dose of LE to RE was 250 mg/kg. The results suggest that antioxidant effects of LF could attenuate the severity of reflux esophagitis and prevent the esophageal mucosal damage, and validate its therapeutic use in esophageal reflux disease.