AIM To study the peripheral mechanism of the inhibitory effect of intra third ventricular administration (icv) of histamine (HA) on gastric acid secretion in rats. METHODS Gastric acid was continuously washed wit...AIM To study the peripheral mechanism of the inhibitory effect of intra third ventricular administration (icv) of histamine (HA) on gastric acid secretion in rats. METHODS Gastric acid was continuously washed with 37℃ saline by a perfusion pump in male adrenalectomized SD rats. Drugs were injected intravenously (iv) by a syringe pump and their effect on pentagastrin induced (10μg·kg·h, iv) gastric acid secretion was observed. RESULTS The inhibitory effect of HA (1μg, icv) on gastric acid secretion was blocked by subdiaphragmatic vagotomy, and pretreatment with atropine (0 005mg·kg·h, iv). Pretreatment with somatostatin antagonist, cyclo [7 aminoheptanoyl Phe D Trp Lys Thr(Bzl)], ( 2μg - 4μg ·kg· 100min , iv) could also block the inhibitory effect of HA on gastric acid secretion in a dose dependent manner. CONCLUSION The inhibitory effect of centrally administrated HA on gastric acid secretion may be mediated by vagi, acetylcholine M receptor and somatostatin.展开更多
AIM To assess the relationship between gastric acid output (GAO) and both pattern of gastroesophageal reflux (GER) and esophageal lesions, and to evaluate the role of GAO and other potential pathogenetic factors in t...AIM To assess the relationship between gastric acid output (GAO) and both pattern of gastroesophageal reflux (GER) and esophageal lesions, and to evaluate the role of GAO and other potential pathogenetic factors in the development of esophagitis. METHODS Gastric acid secretory testing and 24 h intraesophageal pH monitoring were performed in 31 patients with esophagitis and concomitant duodenal ulcer (E+DU) and compared with those of 72 patients with esophagitis (E) alone. RESULTS The GAO in patients with E+DU was significantly higher than in patients with E ( P <0 05). There was no significant difference between the two groups of patients as to endoscopicl findings and parameters of GER ( P >0 05). A multiple regression analysis with stepwise deletion showed that the pre sence of hiatal hernia (HH), GER in upright position and age appeared to correlate significantly with the presence of esophagitis. CONCLUSIONS No parallel relationship between GAO and severity of GER or esophageal lesions exists in patients with E+DU, and that GAO is not a major pathogenetic factor in GER disease.展开更多
目的 探讨电针足阳明胃经原穴足三里穴对胃酸分泌的调节作用及机制。 方法 采用完全随机方法分组。在清醒状态下电针大鼠足三里穴,并与空白对照组及非经非穴组相对比,在针刺不同时间点测胃酸分泌及取血,放免法检测胃液及血浆促胃液素(G...目的 探讨电针足阳明胃经原穴足三里穴对胃酸分泌的调节作用及机制。 方法 采用完全随机方法分组。在清醒状态下电针大鼠足三里穴,并与空白对照组及非经非穴组相对比,在针刺不同时间点测胃酸分泌及取血,放免法检测胃液及血浆促胃液素(GAS)和表皮生长因子(EGF)浓度。 结果 电针足三里穴后空腹胃液量显著减少(P<0.01)pH值上升(P<0.05),酸度变化不大。足三里穴组胃液及血浆GAS浓度均降低,分别为239ng/L±61ng/L vs 294ng/L±32ng/L(P<0.05)和81ng/L±22ng/L vs 102ng/L±30ng/L(P<0.01)。胃液EGF浓度显著升高3.16μg/L±1.05μg/L vs 1.65μg/L±0.35μg/L(P<0.01)。血浆EGF浓度显著降低0.25μg/L±0.01μg/L vs 0.54μg/L±0.11μg/L(P<0.01)。其他组无显著变化。 结论 电针足三里穴明显抑制胃酸分泌并使胃液pH升高,与血浆、胃液GAS下降有关;电针足三里穴诱导上消化道EGF分泌增加,EGF参与抑制胃酸分泌,具有重要意义。展开更多
Despite advances in treatment and the declining incidence,gastric cancer remains the second leading cause of cancer-related deaths in the world.Understanding the progression from inflammation to cancer in the stomach ...Despite advances in treatment and the declining incidence,gastric cancer remains the second leading cause of cancer-related deaths in the world.Understanding the progression from inflammation to cancer in the stomach is crucial in the development of novel therapies and strategies for treating this disease.Chronic inflammation of the stomach is typically caused by Helicobacter pylori(H.pylori)and resulting lesions may lead to gastric cancer.During the progression from inflammation to cancer,the stomach epithelium changes with evidence of the disruption of normal epithelial cell differentiation and infiltrating inflammatory cells.Coincident with the development of atrophic gastritis and metaplasia,is the loss of the gastric morphogen Sonic Hedgehog(Shh).Given its critical role as a regulator of gastric tissue homeostasis,the disruption of Shh expression during inflammation correlates with the loss of normal epithelial cell differentiation,but this has only recently been rigorously tested in vivo using a unique mouse model of targeted gastric Shh deletion.While pre-neoplastic lesions such as atrophic gastritis and in-testinal metaplasia are associated with the loss of Shh within the acid-secreting glands of the stomach,there is a clear link between elevated Shh and signaling to gastric cancers.The current review focuses on the effects of aberrant Shh expression and its role in the development of gastric cancer,specifically in response to H.pylori infection.展开更多
文摘AIM To study the peripheral mechanism of the inhibitory effect of intra third ventricular administration (icv) of histamine (HA) on gastric acid secretion in rats. METHODS Gastric acid was continuously washed with 37℃ saline by a perfusion pump in male adrenalectomized SD rats. Drugs were injected intravenously (iv) by a syringe pump and their effect on pentagastrin induced (10μg·kg·h, iv) gastric acid secretion was observed. RESULTS The inhibitory effect of HA (1μg, icv) on gastric acid secretion was blocked by subdiaphragmatic vagotomy, and pretreatment with atropine (0 005mg·kg·h, iv). Pretreatment with somatostatin antagonist, cyclo [7 aminoheptanoyl Phe D Trp Lys Thr(Bzl)], ( 2μg - 4μg ·kg· 100min , iv) could also block the inhibitory effect of HA on gastric acid secretion in a dose dependent manner. CONCLUSION The inhibitory effect of centrally administrated HA on gastric acid secretion may be mediated by vagi, acetylcholine M receptor and somatostatin.
文摘AIM To assess the relationship between gastric acid output (GAO) and both pattern of gastroesophageal reflux (GER) and esophageal lesions, and to evaluate the role of GAO and other potential pathogenetic factors in the development of esophagitis. METHODS Gastric acid secretory testing and 24 h intraesophageal pH monitoring were performed in 31 patients with esophagitis and concomitant duodenal ulcer (E+DU) and compared with those of 72 patients with esophagitis (E) alone. RESULTS The GAO in patients with E+DU was significantly higher than in patients with E ( P <0 05). There was no significant difference between the two groups of patients as to endoscopicl findings and parameters of GER ( P >0 05). A multiple regression analysis with stepwise deletion showed that the pre sence of hiatal hernia (HH), GER in upright position and age appeared to correlate significantly with the presence of esophagitis. CONCLUSIONS No parallel relationship between GAO and severity of GER or esophageal lesions exists in patients with E+DU, and that GAO is not a major pathogenetic factor in GER disease.
文摘目的 探讨电针足阳明胃经原穴足三里穴对胃酸分泌的调节作用及机制。 方法 采用完全随机方法分组。在清醒状态下电针大鼠足三里穴,并与空白对照组及非经非穴组相对比,在针刺不同时间点测胃酸分泌及取血,放免法检测胃液及血浆促胃液素(GAS)和表皮生长因子(EGF)浓度。 结果 电针足三里穴后空腹胃液量显著减少(P<0.01)pH值上升(P<0.05),酸度变化不大。足三里穴组胃液及血浆GAS浓度均降低,分别为239ng/L±61ng/L vs 294ng/L±32ng/L(P<0.05)和81ng/L±22ng/L vs 102ng/L±30ng/L(P<0.01)。胃液EGF浓度显著升高3.16μg/L±1.05μg/L vs 1.65μg/L±0.35μg/L(P<0.01)。血浆EGF浓度显著降低0.25μg/L±0.01μg/L vs 0.54μg/L±0.11μg/L(P<0.01)。其他组无显著变化。 结论 电针足三里穴明显抑制胃酸分泌并使胃液pH升高,与血浆、胃液GAS下降有关;电针足三里穴诱导上消化道EGF分泌增加,EGF参与抑制胃酸分泌,具有重要意义。
基金Supported by American Cancer Society Research Scholar Award,No.119072-RSG-10-167-01-MPC(to Zavros Y)
文摘Despite advances in treatment and the declining incidence,gastric cancer remains the second leading cause of cancer-related deaths in the world.Understanding the progression from inflammation to cancer in the stomach is crucial in the development of novel therapies and strategies for treating this disease.Chronic inflammation of the stomach is typically caused by Helicobacter pylori(H.pylori)and resulting lesions may lead to gastric cancer.During the progression from inflammation to cancer,the stomach epithelium changes with evidence of the disruption of normal epithelial cell differentiation and infiltrating inflammatory cells.Coincident with the development of atrophic gastritis and metaplasia,is the loss of the gastric morphogen Sonic Hedgehog(Shh).Given its critical role as a regulator of gastric tissue homeostasis,the disruption of Shh expression during inflammation correlates with the loss of normal epithelial cell differentiation,but this has only recently been rigorously tested in vivo using a unique mouse model of targeted gastric Shh deletion.While pre-neoplastic lesions such as atrophic gastritis and in-testinal metaplasia are associated with the loss of Shh within the acid-secreting glands of the stomach,there is a clear link between elevated Shh and signaling to gastric cancers.The current review focuses on the effects of aberrant Shh expression and its role in the development of gastric cancer,specifically in response to H.pylori infection.
