Kolkman J J, Groeneveld A B, Meuwissen S G
Department of Gastroenterology, Free University Hospital, Amsterdam, The Netherlands.
Gut. 1994 Jun;35(6):737-41. doi: 10.1136/gut.35.6.737.
A high intragastric PCO2 (iPCO2), determined tonometrically, is the main factor participating in a low gastric intramucosal pH (pHi) and may point to gastric mucosal ischaemia. iPCO2 might also increase, however, after buffering of gastric acid by bicarbonate; the magnitude of this effect and the efficacy of H2 blockers to prevent it are unclear. Ten healthy volunteers (20-24 years) were studied at baseline and after oral ingestion of 500 mg sodium bicarbonate. The same test was carried out one hour after intravenous injection of 100 mg ranitidine. A glass pH electrode for continuous gastric juice pH measurements and a Tonomitor catheter were placed 10 cm distally from the gastro-oesophageal junction. iPCO2 was measured in saline boluses, infused at 30 minute intervals in the balloon at the tip of the Tonomitor. Before ranitidine was given, basal iPCO2 (mean (SD)) was 8.40 (2.53) kPa, and increased to 19.20 (5.87) kPa after sodium bicarbonate (p < 0.001). After ranitidine, the gastric juice pH increased from 1.8 (0.9) to 5.6 (1.3) (p < 0.05), while basal iPCO2 was 5.60 (0.67) kPa (p < 0.01) and did not change after sodium bicarbonate (6.27 (2.67) kPa)). iPCO2 values after acid secretion suppression were similar to those in capillary blood (5.60 (0.40 kPa)). The difference between intragastric and blood PCO2 during normal acid secretion probably results from buffering of gastric acid by gastric bicarbonate, rather than by duodenogastric reflux or saliva entering the stomach. During acid secretion suppression, intragastric equals blood PCO2, even after oral ingestion of sodium bicarbonate. Hence, acid secretion inhibition is mandatory for proper assessment of iPCO2 and pHi as specific measures of the adequacy of gastric mucosal blood flow.
通过张力测定法测得的高胃内二氧化碳分压（iPCO2）是导致胃黏膜内低pH值（pHi）的主要因素，可能提示胃黏膜缺血。然而，在碳酸氢盐缓冲胃酸后，iPCO2也可能升高；这种效应的大小以及H2阻滞剂预防其发生的效果尚不清楚。对10名健康志愿者（20 - 24岁）在基线时以及口服500毫克碳酸氢钠后进行了研究。在静脉注射100毫克雷尼替丁1小时后进行了相同的测试。将用于连续测量胃液pH值的玻璃pH电极和一个Tonomitor导管放置在距胃食管交界处远端10厘米处。每隔30分钟向Tonomitor尖端的气囊内注入生理盐水团注以测量iPCO2。在给予雷尼替丁之前，基础iPCO2（均值（标准差））为8.40（2.53）千帕，在给予碳酸氢钠后升至19.20（5.87）千帕（p < 0.001）。给予雷尼替丁后，胃液pH值从1.8（0.9）升至5.6（1.3）（p < 0.05），而基础iPCO2为5.60（0.67）千帕（p < 0.01），给予碳酸氢钠后未发生变化（6.27（2.67）千帕）。抑制胃酸分泌后的iPCO2值与毛细血管血中的值相似（5.60（0.40千帕））。正常胃酸分泌期间胃内和血液中PCO2的差异可能是由于胃碳酸氢盐对胃酸的缓冲作用，而非十二指肠 - 胃反流或唾液进入胃内所致。在抑制胃酸分泌期间，即使口服碳酸氢钠后，胃内PCO2也等于血液中的PCO2。因此，为了正确评估iPCO2和pHi作为胃黏膜血流充足性的特定指标，抑制胃酸分泌是必要的。
