Forssell H
Department of Surgery II, Sahlgren's Hospital, Gothenburg University, Sweden.
Acta Chir Scand Suppl. 1987;540:1-54.
A method for measurement of human basal and stimulated gastric bicarbonate secretion was developed in the present investigation. The mechanisms involved in the regulation of basal, vagus nerve stimulated as well as fundic distension induced bicarbonate secretion were studied. The investigations were performed in healthy subjects and duodenal ulcer patients, the latter group before and/or after a proximal gastric vagotomy operation. Healthy subjects as well as ulcer patients were premedicated with a histamine H2-receptor antagonist and gastric bicarbonate secretion was determined by use of a gastric perfusion system in combination with computerized continuous recordings of pH and PCO2. The contribution of alkaline saliva to the measured gastric bicarbonate secretion was minimized by continuous salivary suction and correction was made for swallowed saliva by measurement of amylase in the gastric aspirate. A high rate of gastric perfusion facilitated the identification of alkaline duodenogastric reflux and also eliminated its influence on the measurement of gastric bicarbonate secretion. Validation of the measuring system by instillation of small amounts of bicarbonate showed a satisfactory correlation between added and recovered bicarbonate in the range of bicarbonate determinations usually recorded. Decreasing intragastric pH to between 3 and 4 converted all secreted bicarbonate into CO2, but did not affect the measured value of bicarbonate secretion. Vagal stimulation accomplished by sham feeding increased gastric bicarbonate secretion in sixteen healthy subjects from 410 +/- 39 mumol/h to 692 +/- 67 mumol/h (mean +/- SEM, p less than 0.001). This response was independent of intragastric pH in the range of 2 to 7. The muscarinic receptor antagonist, benzilonium bromide, almost abolished the sham feeding response while indomethacin left it nearly unchanged. Nine duodenal ulcer patients had identical basal and vagally stimulated bicarbonate output as healthy subjects. Two months after proximal gastric vagotomy, the basal bicarbonate secretion was significantly increased, whereas the output in response to sham feeding was unaltered. In the early postoperative period, anticholinergics reduced the enhanced basal bicarbonate secretion to a preoperative level. In six healthy subjects, graded fundic distension with a balloon to volumes of 150 ml, 300 ml and 600 ml, each distension period lasting 60 minutes, increased the bicarbonate secretion by 46% (p less than 0.05), 28% (NS) and 84% (p less than 0.05), respectively.(ABSTRACT TRUNCATED AT 400 WORDS)
本研究开发了一种测量人体基础和刺激状态下胃碳酸氢盐分泌的方法。研究了基础状态、迷走神经刺激以及胃底扩张诱导的碳酸氢盐分泌的调节机制。研究在健康受试者和十二指肠溃疡患者中进行,后者在近端胃迷走神经切断术前和/或术后。健康受试者和溃疡患者均预先给予组胺H2受体拮抗剂,并通过胃灌注系统结合pH和PCO2的计算机连续记录来测定胃碳酸氢盐分泌。通过持续唾液抽吸将碱性唾液对测得的胃碳酸氢盐分泌的影响降至最低,并通过测量胃抽吸物中的淀粉酶对吞咽唾液进行校正。高胃灌注率有助于识别碱性十二指肠-胃反流,并消除其对胃碳酸氢盐分泌测量的影响。通过滴注少量碳酸氢盐对测量系统进行验证,结果表明在通常记录的碳酸氢盐测定范围内,添加的碳酸氢盐与回收的碳酸氢盐之间具有良好的相关性。将胃内pH值降至3至4可将所有分泌的碳酸氢盐转化为CO2,但不影响碳酸氢盐分泌的测量值。假饲引起的迷走神经刺激使16名健康受试者的胃碳酸氢盐分泌从410±39μmol/h增加到692±67μmol/h(平均值±标准误;p<0.001)。在2至7的胃内pH范围内,这种反应与胃内pH无关。毒蕈碱受体拮抗剂溴苄乙铵几乎消除了假饲反应,而吲哚美辛使其几乎不变。9名十二指肠溃疡患者的基础和迷走神经刺激的碳酸氢盐输出与健康受试者相同。近端胃迷走神经切断术后两个月,基础碳酸氢盐分泌显著增加,而假饲反应的输出未改变。在术后早期,抗胆碱能药物将增强的基础碳酸氢盐分泌降低到术前水平。在6名健康受试者中,用气囊将胃底分级扩张至150ml、300ml和600ml,每个扩张期持续60分钟,碳酸氢盐分泌分别增加46%(p<0.05)、28%(无显著性差异)和84%(p<0.05)。(摘要截取自400字)