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近十余年来,由于H_2组织胺受体拮抗剂的开发,使消化性溃疡(简称:溃疡病)的治疗发生了革命性改变,不少病人避免了手术治疗而获得痊愈。最近几年,又推出了几种更有效的新药,除了治疗溃疡病外,对急性胃粘膜出血或应激性溃疡也有效。一、溃疡病治疗的药理学基础消化性溃疡的发病机制认为系致溃疡的因素(胃酸过多、胆汁返流、胃蛋白酶、药物、吸烟等)和抗溃疡的因素(粘膜屏障、细胞保护、血液循环、胃肠道激素、上皮生长因子等)二者之间的不平衡,以及个体神经内分泌反应和遗传素质的差异。过去过于强调胃酸和胃蛋白酶的攻击,近来开始重视抗溃疡因素,特别是胃和十二指粘膜屏障,前列腺素的细胞保护作用和局部血液循环因素等。壁细胞有4种受体调控胃酸的分泌,乙酰胆碱、胃泌素和H_2受体的激活促进胃酸分泌,而前列腺素受体的激活则抑制胃酸分泌,保护上皮细胞。胃酸分泌的细胞内机制是钙通道的开放,CAMP第二信使的作用,最后作用于壁细胞的H~+—K~+—ATP酶泵,导致H~+离子的分泌(图1)。
In the recent ten years, the development of H 2 histamine receptor antagonist has revolutionized the treatment of peptic ulcer (referred to as: ulcer disease), and many patients have been cured without surgical treatment. In recent years, several more effective new drugs have been introduced that are effective in treating acute gastric mucosal hemorrhage or stress ulcer in addition to treating ulcer disease. First, the pharmacological treatment of ulcer disease Pathogenesis of peptic ulcer ulcer caused by factors (hyperacidity, bile reflux, pepsin, drugs, smoking, etc.) and anti-ulcer factors (mucosal barrier, cell protection, Blood circulation, gastrointestinal hormones, epidermal growth factor, etc.), as well as individual differences in neuroendocrine response and genetic predisposition. Over the past emphasis on gastric acid and pepsin attacks, recently began to value anti-ulcer factors, especially the gastric and duodenal mucosal barriers, prostaglandin cytoprotection and local blood circulation factors. Parietal cells have four receptors regulate the secretion of gastric acid, the activation of acetylcholine, gastrin and H 2 receptors to promote gastric acid secretion, while the activation of prostaglandin receptors inhibit gastric acid secretion and protect the epithelial cells. The intracellular mechanism of gastric acid secretion is the opening of calcium channels, the second messenger of CAMP, and finally the H ~ + -K ~ + -ATPase pump acting on the parietal cells, leading to the secretion of H ~ + ions (Figure 1).