针刺调控胃酸分泌作用及机制

1 胃酸分泌的调节机制 胃酸分泌受头相、胃相和肠相的各种因素调节。中枢神经系统、外周神经系统(包括肠神经系统)及细胞内信号系统在各期中都发挥重要调节作用,胃粘膜中壁细胞、D细胞、主细胞、G细胞和嗜铬样细胞(ECL)是实现胃酸分泌功能的五大主要细胞,最终泌酸效应依赖于上述细胞间的相互作用。 1.1 中枢神经系统的调节 中枢神经系统内与酸分泌调节相关的主要部位是迷走神经运动背核,下丘脑和孤束核。迷走神经运动背核是中枢刺激的最终整合中枢,破坏此核后,中枢刺激的酸分泌消失;而电刺激该核则产生强的分泌效应,损毁     

电针猫足三里穴对下食管括约肌压力调节功能的影响

[目的]研究电针（EA）猫足三里穴对下食管括约肌压力（LESP）的影响,探讨足三里穴与食管动力调节之间的关系。[方法]将28只健康家猫行内镜检查,确定无镜下食管病（炎）。随机分为足三里穴组、非经非络穴组。应用加拿大E-7-1-1-1-2-5-5-5型8通道细微注水测压管和荷兰UPS-2020型食管测压系统测定猫LESP。[结果]EA猫足三里穴和非经非络穴期间和停止后,LESP较EA前均有显著性升高,足三里穴组EA期间LESP由（16．21±5．49）mmHg（1mmHg=0．133kPa）升高至（23．14±8．81）mmHg（P〈0．01）,EA停止后LESP升至（25．50±6．73）mmHg（P〈0．01）;非经非络穴组EA期间LESP由（15．64±3．61）mmHg升至（18．93土5．57）mmHg（P〈0．01）,EA停止后LESP升至（20．43±5．24）mmHg（P〈0．01）。EA足三里穴对LESP的升高程度在EA期间和停止后均明显高于非经非络穴（P〈0．05）。[结论]EA健康猫足三里穴可以升高LESP,对下食管括约肌具有良性调理功能,其机制尚未完全阐明。     

辣椒素对胃酸分泌的影响及机制

辣椒素(capsaicin,CAP)对胃酸分泌有一定影响,多数研究显示小剂量抑制胃酸分泌,大剂量则可能促进胃酸分泌,甚至报道有些剂量的CAP对胃酸分泌没有影响.CAP对胃酸分泌影响的差异可能与其药理特性有关,不同剂量、不同时期及给药的不同途径对胃酸分泌的影响不同.CAP可能通过直接刺激中枢、外周辣椒素-敏感感觉神经(capsaicin-sensitive sensoryneurons,CSSN)及壁细胞等的辣椒素受体,引起降钙素基因相关肽、P物质、神经激肽A、血管活性肠肽等神经递质的释放,参与胃酸分泌的调节.     

幽门螺杆菌对胃酸分泌的影响

阐述急性及慢性Hp感染对胃酸分泌的影响并探讨Hp感染与胃酸分泌之间的相互作用在十二指肠溃疡发病中的地位及其机制。     

幽门螺杆菌对胃酸分泌的影响

阐述急性及慢性ＨＰ感染对胃酸分泌的影响并探讨ＨＰ感染与胃酸分泌之间的相互作用在十二指肠溃疡发病中的地位及其机制。     

电针足三里穴对应激性胃溃疡大鼠一氧化氮和儿茶酚胺的影响

本文对电针足三里穴抗“束缚－冷冻”应激性胃溃疡大鼠一氧化氮（ＮＯ）、多巴胺（ＤＡ）和去甲肾上腺素（ＮＥ）的含量进行了分析，结果如下：①应激性胃溃疡大鼠血清ＮＯ含量比对照组非常显著下降， Ｐ＜０． ０１，胃窦粘膜ＤＡ含量显著下降， Ｐ＜０． ０５，胃体粘膜ＤＡ呈增高趋势；②电针足三里穴引起应激性胃溃疡大鼠ＮＯ水平回回升，与应激组相比， Ｐ＜０．０１。电针引起胃窦和胃体粘膜ＤＡ、ＮＥ含量改变，有双向调节作用。即原降低者上升、原升高者下降，分别与应激组相比，均为Ｐ＜０． ０１。提示电针对胃粘膜的保护作用是通过对ＤＡ和 ＮＥ的双向调节，发挥了ＤＡ的调控作用，影响ＮＥ的水平，通过ＮＯ的舒血管作用，调节血流量，增强粘膜防御能力而实现的。     

电针足三里穴对兔肺缺血再灌注损伤脂质过氧化反应的影响

目的研究电针足三里穴对在体家兔肺缺血再灌注损伤的影响。方法28只新西兰家兔采用在体肺热缺血再灌注损伤模型．随机分四组（n=7）。A组：假手术组。左开胸游离支气管和肺动脉、静脉后维持通气180min。B组：缺血再灌注组，左开胸游离支气管和肺动脉、静脉后阻断左肺门60min．开放再通气120min。C组：阻断左肺门60min后．开放再通气即刻电针足三里穴旁5mm处30 min．继续双肺通气90min。D组：电针足三里穴＋缺血再灌注组，阻断左肺门60min后。开放再通气即刻电针足三里穴30min．继续双肺通气90min。观察并记录各组动物术中平均动脉压和心率的改变及实验结束时肺组织丙二醛（MDA）和髓过氧化物酶（MPO）含量以及肺组织湿/干重比（W/D）和血气变化。结果各组动物相应时间点的心率比较，均无统计学意义（P〉0.05）。自再灌注30min开始，与B组比较。C组平均动脉压显著降低（P〈0．05），D组平均动脉压与B组比较无统计学意义（P〉0．05）。B组肺组织MDA和MPO含量、W／D及PaCO2值均较A组升高．pH和PaO2值显著降低（P〈0．05或P〈0．01）；D组肺组织MDA和MPO含量、W／D及PaCO2值均较B组降低，pH和PaO2值显著升高（P〈0．05或P〈0．01）。结论电针家兔足三里穴可明显抑制肺缺血再灌注损伤时肺组织MDA和MPO的产生，减轻肺水肿的发生，改善血气变化及酸碱失衡．对在体家兔肺缺血再灌注损伤有一定的保护作用。     

奥美拉唑对十二指肠溃疡患者胃液表皮生长因子浓度的影响

目的 观察奥美拉唑（Ｏｍｅ）愈合十二指肠溃疡（Ｄｕ）对胃液表皮生长因子（ＥＧＦ）浓度的影响。方法 ５８例Ｈｐ阳性Ｄｕ患者随机分为三组：奥美拉唑（Ｏｍｅ）＋胶体铋剂（ＣＢＳ）＋羟氨苄青霉素（Ａｍｏ）组，雷尼替丁（Ｒａ）＋ＣＢＳ＋Ａｍｏ组和ＣＢＳ＋Ａｍｏ组，服药４周（Ｏｍｅ、Ｒａ和ＣＢＳ分别服４周，Ａｍｏ２周）。于治疗前、后分别测定空腹血清胃泌素和胃液ＥＧＦ浓度并与１２例Ｈｐ阴性健康对照组比较。结果：     

表皮生长因子和胃泌素在胃癌组织中的表达及意义

目的 探讨表皮生长因子(EGF)和胃泌素(GAS)在胃癌组织中的表达,及其相互关系与意义.方法 选取我院2003年1月～2009年12月经病理确诊的胃癌(GC)70例,慢性浅表性胃炎(CSG)25例,经过纳入标准及排除标准的筛选而作为研究对象.采用免疫组织化学Envision方法,检测EGF、GAS在各组胃黏膜组织中的...     

Effect of aging on gastric acid secretion,serum gastrin,and antral gastrin content in rats

The purpose of this study was to characterize the effects of aging on gastric acid secretion and on serum and antral concentrations of gastrin in rats. Young and old Fischer 344 rats were prepared with gastric fistulas. Twenty-four hours after surgery, graded doses of human synthetic gastrin-17 (SHG-17) (2, 5, 10, 20, and 40 g/kg) were given intravenously in random order. Gastric secretions were collected for gastric acid measurement before and at 15-min intervals after each dose of gastrin. In a separate study, blood was collected and the stomachs were removed for antral gastrin extraction from fed young and old rats. Serum and antral gastrin was measured by radioimmunoassay. The basal and gastrin-stimulated acid secretions were significantly decreased in aged rats compared to the young rats. The basal acid output was 0.4±0.2 eq/15 min in the aged rats and 1.5±0.5 eq/15 min in the young. The maximal acid output stimulated by gastrin was 11.1±1.8 eq/15 min in the aged rats and 24.2±2.8 eq/15 min in the young. Both serum and antral concentrations of gastrin were significantly decreased in aged rats. Serum gastrin concentration was 114.8±7.4 pg/ml in the aged rats and 192.0±14.4 pg/ml in the young. Antral gastrin concentration was 3.9±0.5 g/g tissue in the aged rats, which was significantly less than the concentration in the young (6.5±0.4 g/g tissue). Antral gastrin content did not change with aging. Gastric acid secretion in aged rats is significantly decreased compared to the young in both the basal condition and in response to fixed doses of exogenous gastrin. Diminished concentrations of circulating gastrin may well be responsible, at least in part, for the diminished acid secretion in the aged rats.Part of this work was presented at the special session on aging during the Digestive Disease Week held by the American Gastroenterology Association (AGA) in New York, May 14, 1985, and has been published in abstract form (Gastroenterology 88:1445, 1985).Supported by grants from the National Institutes of Health (RO1 DK 15241, PO1 DK 35608, RCDA CA 00854, CA 38651) and a grant from the American Cancer Society (PDT-220).     

Effect of acupuncture on gastric acid secretion in healthy male volunteers

Six randomized, placebo controlled studies were performed to investigate the effect of electroacupuncture on gastric acid output in 38 healthy males. Electroacupuncture decreased basal acid output when compared to placebo acupuncture [from 3.50±0.59 mmol/hr to 2.54±0.56 mmol/hr (P<0.05)] as well as sham feeding-stimulated acid output [from 18.52±2.25 mmol/hr to 5.38±2.11 mmol/hr (P<0.005)], but had no effect on the pentagastrin stimulated acid output. The inhibitory effect of acupuncture on sham feeding-stimulated acid output was not affected by local anesthesia of the acupoint, but was prevented by a prior intravenous naloxone injection. Acupuncture did not alter plasma gastrin levels (20.7±7.6 g/liter, vs control 21.2±7.2 g/liter) but naloxone increased it (26.1±14.5 g/liter) (P<0.05). We conclude that the antisecretory effects of electroacupuncture do not result from decreased gastrin release or decreased parietal cell sensitivity to gastrin, but are mediated through naloxone-sensitive opioid neural pathways and vagal efferent pathways.Dr. Tougas was supported by a Fellowship of the Medical Research Council of Canada.This work was presented in part at the Annual Meeting of The American Gastroenterological Association, New Orleans, May 1988; Washington, May 1989; and San Antonio, May 1990.     

健中愈疡片对乙酸诱导胃溃疡大鼠表皮生长因子及其受体表达的影响

[目的]观察健中愈疡片对乙酸诱导胃溃疡大鼠血清表皮生长因子（EGF）水平和胃溃疡边缘表皮生长因子受体（EGFR）表达的影响。[方法]制备乙酸诱导大鼠胃溃疡模型，分别予健中愈疡片、雷尼替丁和0．85％氯化钠液治疗14d，用放射免疫分析法测定大鼠血清EGF水平，免疫组织化学染色法检测胃溃疡边缘EGFR表达。[结果]造模3d时，胃溃疡模型组大鼠的血清EGF水平明显高于正常对照组，胃溃疡边缘EGFR表达比正常对照组明显增加。治疗14d后，与雷尼替丁组和0．85％氯化钠液组比较，健中愈疡片组的血清EGF水平显著减少（P〈0．01），而胃溃疡边缘EGFR表达显著增加（P〈0．01）。[结论]血清EGF水平可以作为反映胃肠黏膜完整性的一个监控指标，健中愈疡片能够减少血清EGF水平和增加胃溃疡边缘EGFR表达，这可能是其加速乙酸诱导胃溃疡愈合的主要作用机制。     

促愈颗粒对胃溃疡实验大鼠胃黏膜表皮生长因子及其受体表达的影响

[目的]研究促愈颗粒对乙酸烧灼型胃溃疡(GU)大鼠胃黏膜表皮生长因子(EGF)及其受体(EGFR)表达的影响。[方法]将大鼠随机分为4组:正常对照组,模型组,促愈颗粒组和雷尼替丁组。乙酸制备慢性GU大鼠模型后,于给药14 d和28 d后分2次处死大鼠,观察胃黏膜组织形态,免疫组织化学技术检测大鼠胃黏膜EGF及EGFR水平。[结果]与模型组比较,促愈颗粒组和雷尼替丁组囊状扩张腺体数量均显著减少(P<0.01,<0.05),EGF及EGFR水平均显著增高(P<0.01,<0.05),且促愈颗粒组作用均优于雷尼替丁组(均P<0.05)。[结论]促愈颗粒可能通过增加胃黏膜EGF和EGFR的水平,进而提高GU再生黏膜结构和功能成熟度,从而促进溃疡愈合,提高溃疡愈合质量,并防止溃疡复发。     

Study on content of serum epidermal growth factor,gastric acid secretion and serum gastrin in duodenitis

AIM: To study whether there is EGF secreting abnormality in duodenitis and its relationship with gastric acid output and serum gastrin, so as to further explore the pathogenesis of duodenitis. METHODS: Twenty-five duodenitis patients were confirmed by electrogastroscopy and biopsy, with an average age of 35.9 ± 7.0 years (range, 24-52 years). The control group consisted of 20 healthy volunteers (10 females, 10 males), with an average age of 34.4 ± 7.6 years (range, 23-48 years). Twenty duodenal ulcer patients (10 females, 10 males), with an average age of 35.0 ± 7.6 years (range, 24-52 years), were also included. Serum EGF and gastrin were measured using radioimmunoassay. Intragastric acidity was determined by pentagastrin method. Statistical analysis was performed using Student’s t-test. RESULTS: In comparison with those in the control group, the contents of serum EGF and serum gastrin in duodenitis patients were all significantly increased. In comparison with those in the duodenal ulcer group, serum EGF was significantly increased, basal acid output and peak acid output were decreased, and serum gastrin was increased significantly in duodenitis patients. Serum EGF was negatively correlated with gastric acid output and positively correlated with serum gastrin. CONCLUSION: In duodenitis, serum EGF concentration was increased, which was positively correlated with serum gastrin content, but was negatively correlated with gastric acid output. This indicates that EGF plays a protective role in the pathogenesis of duodenitis, which provides a new clue to pathogenesis study of duodenitis.     

Verapamil decreases ethanol-induced gastric acid secretion in rats

The present study examined the effect of verapamil, a calcium channel blocker, on gastric acid secretion and circulating gastrin levels in rats after ethanol challenge. Normal saline or verapamil were given intraperitoneally to different groups of rats at 1 min, 1 h or 2 h before the administration of ethanol. One hour later, gastrin and gastric acid concentrations were determined. Regression analysis revealed the relationship between gastric acid output and serum gastrin levels in the group receiving saline intraperitoneally and ethanol orogastrically and the group receiving saline both intraperitoneally and orogastrically is similar. The slope of the regression line of the ethanol-challenged group treated with verapamil, however, was significantly lower than the slopes of the other two groups (P less than 0.001). Furthermore, verapamil decreased gastrin levels and acid output significantly in the ethanol-challenged group (P less than 0.01). When given 10 min prior to ethanol challenge, verapamil had a greater acid suppression effect than when given 60 or 120 min before the challenge. Verapamil at 20 mg/kg was more effective in acid secretion than at 10 mg/kg bodyweight, when administered 60 min before ethanol challenge.     

Intestinal fat digestion plays a significant role in fat-induced suppression of gastric acid secretion and gastrin release in the rat

We have investigated the role of intestinal fat digestion in fat-induced suppression of gastric acid secretion and gastrin release in the rat. Intraduodenal administration of oleic acid (10%, pH 6.5) and triglyceride (10%, pH 6.5) at a rate of 2 ml/hr resulted in significant suppression of gastric acid secretion and gastrin release stimulated by intragastric perfusion of peptone (0.5%). Diversion of pancreatic juice from the duodenum completely abolished triglyceride-induced inhibition of peptone-stimulated gastric acid secretion and plasma gastrin release, but oleic acid-suppressed gastric acid secretion and gastrin release were unaffected by pancreatic juice diversion. Intraduodenal administration of digested triglyceride, prepared by preincubation with lipase, caused significant suppression of the peptone-induced gastric acid secretion and rise in plasma gastrin levels, even though pancreatic juice was excluded. The results of this study indicate that digestive products of triglyceride by pancreatic juice, especially by lipase, are responsible for the intestinal fat-induced inhibition of gastric acid secretion and gastrin release and that intestinal fat digestion plays a significant role in the mechanism.Part of this work was presented at the Annual Meeting of the American Gastroenterological Association, May 19–22, 1991, New Orleans, and appeared in abstract form inGastroenterology 100:A160, 1991.     

Protection of gastric mucosa from ethanol induced injury by recombinant epidermal growth factor in rats

ＮＴＲＯＤＵＣＴＩＯＮＥｐｉｄｅｒｍａｌｇｒｏｗｔｈｆａｃｔｏｒ（ＥＧＦ）ｉｓａｓｉｎｇｌｅｃｈａｉｎｐｏｌｙｐｅｐｔｉｄｅｔｈａｔｉｓｓｅｃｒｅｔｅｄｂｙｓｕｂｍａｎｄｉｂｕｌａｒａｎｄＢｒｕｎｎｅｒ′ｓｇｌａｎｄｓａｎｄｉｓａｐｏｗｅｒｆｕｌｍ...     

Significance and regulation of gastric secretion of platelet-activating factor (PAF-Acether) in man

Platelet-activating factor (PAF) has been implicated in the pathogenesis of acute inflammatory and ulcerative diseases of the upper gastrointestinal tract. In the present study, we compared the gastric output of PAF and its precursors with gastric acid output, in patients with various upper gastrointestinal tract diseases and healthy controls. PAF and precursors were also extracted from gastric biopsies from subjects with chronic gastritis and/or gastric colonization byHelicobacter pylori. Under basal conditions, hourly gastric PAF output increased in esophagitis and erosive gastritis, but not in duodenal ulcer or Zollinger-Ellison syndrome. In the gastric juice of duodenal ulcer patients, PAF output rose after secretin, but in patients with Zollinger-Ellison syndrome, PAF was only detected when gastric acid secretion had been reduced by antisecretory drugs and no concurrent changes were observed in serum gastrin levels. After pentagastrin, patients and controls exhibited a significant decrease in PAF output and a negative correlation was found between PAF and acid outputs (r=–0.57,p<0.01). When PAF was incubated with gastric juicein vitro, it underwent degradation irrespective of the medium pH. We found no relation between the outputs of PAF and precursors and the severity of gastritis or gastric colonization byH. pylori. Overall, these results suggest that PAF might be released in the stomach by gastric epithelial cells and could be responsible for mucosal injury of the upper gastrointestinal tract.     

Cholecystokinin is not a physiological regulator of gastric pepsin secretion in rats

The physiological relevance of cholecystokinin (CCK) in gastric pepsin secretion is unclear, although CCK has been reported to stimulate pepsin secretion in intact animals and in dispersed chief cell. To clarify the physiological role played by this peptide in pepsin secretion, we determined the effects of intravenous infusions of CCK on gastric pepsin release, and investigated the effect of endogenous CCK released by small amounts of trypsin inhibitor on pepsin secretion in conscious rats. The infusion of CCK-8 at 1 nmol/kg per h resulted in a plasma CCK concentration of 204 pM and a 2.5-fold increase in pepsin secretion compared to the baseline rate. The infusion of CCK-8 at 0.3 nmol/kg per h resulted in a plasma CCK concentration of 41.8 pM and also caused a significant increase in pepsin secretion compared to the baseline rate. However, the infusion of CCK-8 at 0.1 nmol/kg per h (plasma CCK level, 19.9 pM), which is still far beyond the physiological plasma levels of CCK, did not significantly affect pepsin secretion. In addition, the intraduodenal infusion of soybean trypsin inhibitor increased the plasma CCK concentration to 4.4 pM, a value comparable to that observed after feeding (3.3 pM), but again, this had no effect on gastric pepsin secretion. We conclude that CCK is not a physiological regulator of gastric pepsin secretion in rats.