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。     

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     

去氧胆酸钠损伤胃粘膜引起胃酸分泌改变机制的研究

我们在研究去氧胆酸钠(DOC)损伤胃牯膜后的修复机制时，发现胃分泌的改变对胃粘膜损伤修复有重要影响。NO，作为一种胃粘膜保护性物质，在胃牯膜损伤后即见增高，因而本探讨NO与胃酸分泌改变的关系。     

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。     

胃酸分泌胃壁细胞信号转导机制研究进展

随着细胞生物学、分子生物学和各种显微研究技术的不断完善，对胃壁细胞泌酸机制的了解也有了长足的进步，文章对胃酸分泌胃壁细胞的细胞信号转导机制研究进展作一综述。     

年龄与胃酸分泌

本文提出了胃酸分泌不随年龄增长而降低的这一与传统观念相反的观点，本文试验表明幽门螺杆菌总感染率老年组为５７．１％，青年组１３．６％，感染者易致慢性活动性胃炎，最终发展成萎缩性胃炎，胃粘膜萎缩是影响胃酸分泌的一个重要因素，胃泌素随年龄增长而升高，它刺激壁细胞分泌胃酸。     

老年胃酸分泌与生长抑素的研究

目的探讨老年胃泌酸功能与生长抑素的调节机制．方法我室应用ＲＩＡ法对２０例老年人和１５例青年人胃液及９只Ｗｉｓｔａｒ老年鼠，２０只青年鼠胃粘膜组织、血浆生长抑素含量进行测定，以及对老年人和青年人进行胃酸分泌试验．结果老年人组比青年组胃液生长抑素呈高水平分泌，空腹胃液ＳＳ为（１３６５±４４３）ｎｇ／Ｌｖｓ（８５９±３４５）ｎｇ／Ｌ，Ｐ＜００１；刺激后ＳＳ为（１９６７±６６４）ｎｇ／Ｌｖｓ（１１４１±１０７３）ｎｇ／Ｌ，Ｐ＜００１．老年人比青年人胃酸分泌量明显减少，ＢＡＯ为（３５±２１）ｍｍｏｌ／ｈｖｓ（６９±４４）ｍｍｏｌ／ｈ，Ｐ＜００１；ＰＡＯ为（１３６±６４）ｍｍｏｌ／ｈｖｓ（２０８±１１２）ｍｍｏｌ／ｈ，Ｐ＜００５．不同年龄Ｗｉｓｔａｒ大鼠胃粘膜组织生长抑素具有不同的生理浓度，在老龄鼠比青年鼠ＳＳ也呈高水平分布，为（４５２５±１８４２）ｎｇ／ｇ蛋白ｖｓ（１５０９±９３８）ｎｇ／ｇ蛋白，Ｐ＜００１．结论老年胃泌酸功能改变与生长抑素调节作用存在重要关系．     

辣椒素对胃动力的影响及其机制

辣椒素(capsaicin,CAP)药理作用广泛,其对胃动力的影响已引起消化学者的关注.多数研究认为小剂量的CAP可促进胃动力,一定剂量范围的CAP可调节胃动力,而大剂量CAP对胃动力可能有抑制作用.CAP对胃动力的作用机制可能与CAP受体(vanilloid receptor subtype l,VRl)、P物质(SP)、乙酰胆碱、神经激肽A、生长激素释放肽和钙离子等有关.CAP可能成为一种有前景的胃动力新药.     

辣椒素对内脏痛觉过敏的影响及其机制

辣椒素(capsaicin,CAP)药理作用广泛,其对内脏痛觉过敏(visceral hyperalgesia,VHL)的影响已引起广大学者的关注.研究显示小剂量CAP可能诱发VHL,而大剂量的CAP可能对VHL有抑制作用.CAP对VHL的作用机制可能与CAP受体(vanilloid receptor subtype 1,VR1)及其VR1的磷酸化和去磷酸化、P物质(SP)、降钙素基因相关肽(CGRP)、蛋白水解酶激活型受体2(protease-activated receptor 2,PAR2)等有关.CAP可能成为一种有前景的治疗VHL的新药.     

辣椒素对胃黏膜的作用及其机制

辣椒素(capsaicin)、辣椒素敏感传入神经元(CSAN)及辣椒素受体(VR1)与胃黏膜损伤及修复密切地相关.研究显示辣椒素对胃黏膜具有保护作用,可能与其增加胃黏膜血流、促进胃动力、调节胃酸和前列腺素分泌等因素有关.本文对辣椒素对胃黏膜的作用及其机制的研究进展进行综述.     

GABA-mimetic effect on gastric acid secretion. Possible significance in central mechanisms

Parenteral administration of beta-(p-chlorophenyl)-gamma-aminobutyric acid (PCP-GABA), a lipophilic GABA mimetic, has been shown to aggravate stress-induced ulcerations in the rat. Since acid hypersecretion may be a possible mechanism for this, we studied the effect of graded doses of PCP-GABA on rat gastric acid secretion. The stimulatory effect of PCP-GABA was found to be dose-dependent, long-acting, and massive, exceeding the maximal effects of histamine and bethanechol. The acid stimulant effect of PCP-GABA was completely abolished not only by atropine but also by truncal vagotomy. Vagotomized, PCP-GABA-treated animals responded to bethanechol, suggesting that a peripheral (cellular) mechanism is not involved. We conclude that PCP-GABA acts centrally to activate vagal centers and to cause acid hypersecretion. Although hypersecretion of acid caused by PCP-GABA may be involved in the observed aggravation of stress-induced ulceration in the rat stomach, evidence for this has yet to be provided.     

Effects of pentoxifylline on alcohol-induced gastric injury and acid secretion in rats

We aimed to evaluate the protective effects of pentoxifylline on alcohol-induced gastric injury, its relation with nitric oxide and prostaglandin synthesis, as well as gastric acidity in rats. Acute gastric mucosal injury was induced by intragastric infusion of 2 ml 98% alcohol. Pentoxifylline was given at 100 mg/kg intraperitoneally. Indomethacin and N^G-nitro-L arginine were used to inhibit prostaglandin and nitric oxide synthesis, respectively. Macroscopic and microscopic gastric injuries were evaluated. Gastric pH, tissue malondialdehyde levels, oxidized and reduced glutathion (GSSG/GSH) levels, and effects of pentoxifylline on gastric acid output were measured. Pentoxifylline pretreatment significantly reduced macroscopic and microscopic gastric injury. Malondialdehyde level was lower in pentoxifylline treated rats (351.1 ± 94.1 nmol/g vs 624.3 ± 234.2 nmol/g). Pentoxifylline has a protective role on alcohol-induced gastric mucosal injury in rats. This effect is not related to synthesis of prostaglandins and changes in gastric acidity but does seem to be related to nitric oxide-mediated pathways. In contrast, pentoxifylline increases gastric acid output significantly.     

Specific beta-adrenergic mechanisms in the hypoglycaemic activation of gastrin and gastric acid secretion

To study whether specific beta-adrenergic mechanisms contribute to the hypoglycaemic activation of gastrin and gastric acid secretion, the effects of racemic and dextroisomer propranolol (0.1 mg/kg, intravenously) were studied during insulin tests (0.2 IU/kg) in 13 persons. dl-Propranolol inhibited the gastrin response to hypoglycaemia markedly and more than the insignificant alteration observed after d-propranolol. Gastric acid response to hypoglycaemia was significantly reduced by dl-propranolol and not by d-propranolol. The findings demonstrate that non-beta-adrenergic effects of propranolol on the stomach are minor and that specific beta-adrenergic mechanisms are directly or indirectly involved in the hypoglycaemic stimulation of the stomach.     

Ghrelin and gastric acid secretion

Ghrelin, a novel growth hormone-releasing peptide, was originally isolated from rat and human stomach. Ghrelin has been known to increase the secretion of growth hormone （GH）, food intake, and body weight gain when administered peripherally or centrally. Ghrelin is also known to stimulate the gastric motility and the secretion of gastric acid. In the previous studies, the action of ghrelin on acid secretion was shown to be as strong as that of histamine and gastrin in in-vivo experiment. In the studies, the mechanism for the action of ghrelin was also investigated. It was shown that vagotomy completely inhibited the action of ghrelin on the secretion of gastric acid suggesting that vagal nerve is involved in the mechanism for the action of ghrelin on acid secretion. As famotidine did not inhibit ghrelin-in- duced acid secretion in the study by Masuda et al, they concluded that histamine was not involved in the action of ghrelin on acid secretion. However, we have shown that famotidine completely inhibited ghrelin-induced acid secretion and histidine decarboxylase （HDC） mRNA was increased in gastric mucosa by ghrelin injection which is inhibited by vagotomy Our results indicate that histamine is involved in the action of ghrelin on acid secretion. Furthermore synergistic action of gastrin and ghrelin on gastric acid secretion was shown. Although gastrin has important roles in postprandial secretion of gastric acid, ghrelin may be related to acid secretion during fasting period or at night. However, further studies are needed to elucidate the physiological role of ghrelin in acid secretion.