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
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
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。
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.
