Division of Gastroenterology, University Hospital Dubrava, Zagreb, Croatia.
Dig Dis. 2011;29(5):444-53. doi: 10.1159/000331512. Epub 2011 Nov 16.
The story of gastric acid secretion began with early ideas on gastric secretion (Spallanzani and de Réaumur, 17th century) and with first descriptions of food digestion (Dupuytren and Bichat, Beaumont, early 18th century), followed by proof that gastric juice contained acid (Prout, early 18th century). The research continued with first descriptions of gastric glands as the source of gastric acid and its changes upon digestive stimulus (Purkinje and Golgi, mid and late 19th century). The theory of 'nervism' - the neuro-reflex stimulation of gastric secretion by vagal nerve (Pavlov, early 20th century) was contrasted by a histamine-mediated concept of gastric secretion (Popielski and Code, mid 20th century). Thus, gastric acid and pepsin (Schwann, early 19th century) were found to be essential for food digestion and studies also pointed to histamine, being the most potent final common chemostimulator of oxyntic cells. The discoveries in etiopathogenesis of mucosal injury were marked by the famous dictum: 'No acid, no ulcer' ('Ohne saueren Magensaft kein peptisches Geschwür', Schwarz, 1910) that later induced the term of 'mucosal defense' and the notion that the breaking of 'gastric mucosal barrier' represents the initial step in the process of mucosal injury (Davenport, Code and Scholer, mid 20th century). The prostaglandins were shown to influence all major components of gastric mucosal barrier, described with the term 'cytoprotection' (Vane, Robert and Jacobson, 1970s). Beginning in the latter half of 19th century, the studies on gastric bacteriology that followed enabled the discovery of association between Campylobacter (Helicobacter) pylori and peptic ulcers (Warren and Marshall, 1980s) that led to worldwide major interventions in treating peptic ulcer disease. The surgical approach to peptic ulcer had been outlined by resection procedures (Billroth, Pean, Moynihan, late 19 century) and vagotomy, with or without drainage procedures (Jaboulay, Latarjet, Dragstedt, mid 20th century). Antacids, protective agents, anticholinergics, and later gastrin antagonists and prostaglandins were used for decades in the treatment of peptic ulcer, with differing effects. The advent of the concept of H(2)-receptor antagonists (Black, 1970s) and the discovery of acid (proton) pumps in parietal cells (Ganser, Forte and Sachs, late 1970s) paved the way for potent (H(2) antagonists) and profound acid inhibition (proton pump inhibitors) that revolutionized the treatment of acid-related disorders, including peptic ulcer disease. Worldwide, peptic ulcer and its complications remain the cause of significant morbidity, especially in older age groups, representing a major burden for ambulatory and hospital healthcare resources.
胃酸分泌的故事始于早期对胃酸分泌的认识（斯帕兰扎尼和雷蒙，17 世纪）以及对食物消化的初步描述（迪皮特朗和比沙，18 世纪初），随后证明胃液中含有酸（普劳特，18 世纪初）。研究继续描述胃腺是胃酸的来源及其在消化刺激下的变化（珀金杰和高尔基，19 世纪中叶和晚期）。“神经主义”理论——迷走神经对胃酸分泌的神经反射刺激（巴甫洛夫，20 世纪初）与组胺介导的胃酸分泌概念形成对比（波皮耶尔斯基和科德，20 世纪中叶）。因此，胃酸和胃蛋白酶（施旺，19 世纪初）被发现是食物消化所必需的，研究还指出，组胺是刺激泌酸细胞的最有效终末共同化学刺激物。黏膜损伤发病机制的发现以著名的格言为标志：“无酸无溃疡”（“Ohne saueren Magensaft kein peptisches Geschwür”，施瓦兹，1910 年），后来这一术语被称为“黏膜防御”，并提出“胃黏膜屏障破裂”是黏膜损伤过程的初始步骤（达文波特、科德和肖勒，20 世纪中叶）。前列腺素被证明影响胃黏膜屏障的所有主要成分，并用“细胞保护”一词来描述（瓦恩、罗伯特和雅各布森，20 世纪 70 年代）。从 19 世纪下半叶开始，对胃细菌学的研究发现了幽门螺杆菌（弯曲杆菌）与消化性溃疡之间的关联（沃伦和马歇尔，20 世纪 80 年代），这导致了全球范围内对消化性溃疡病治疗的重大干预。消化性溃疡的手术方法包括切除术（比尔罗特、皮安、莫尼汉，19 世纪末）和迷走神经切断术，伴或不伴引流术（雅布赖、拉塔热、德拉格斯特德，20 世纪中叶）。抗酸剂、保护剂、抗胆碱能药物，以及后来的胃泌素拮抗剂和前列腺素，在过去几十年中被用于治疗消化性溃疡，但效果不同。H2 受体拮抗剂（布莱克，20 世纪 70 年代）和壁细胞质子泵（甘瑟、福尔特和萨克斯，20 世纪 70 年代末）的发现为强效（H2 拮抗剂）和深度抑酸（质子泵抑制剂）铺平了道路，彻底改变了酸相关疾病的治疗方法，包括消化性溃疡病。在全球范围内，消化性溃疡及其并发症仍然是导致发病率显著的原因，尤其是在老年人群中，这给门诊和医院医疗资源带来了重大负担。
