Kolkman J J, Groeneveld A B, Meuwissen S G
Department of Gastroenterology, Medisch Spectrum Twente, Enschede, The Netherlands.
J Crit Care. 1999 Mar;14(1):34-8. doi: 10.1016/s0883-9441(99)90006-0.
The tonometric detection of a high intragastric regional P(CO2) (PrCO2) reflecting an elevated intramucosal P(CO2) can be helpful to diagnose mucosal ischemia, if acid secretion is suppressed to avoid intragastric CO2 production through buffering of acid by bicarbonate in the stomach. It is recommended to perform tonometry in the fasting state, but this may hamper feeding of the critically ill. On the other hand, postfeeding tonometry could serve as a diagnostic stress test because feeding increases mucosal blood flow demand, provided that the meal itself does not hamper diffusion of CO2 from mucosa to tonometer balloon and does not generate intragastric CO2, independently from intramucosal P(CO2). We therefore studied the effect of a standard meal on intragastric PrCO2 tonometry in healthy volunteers with suppression of meal-stimulated gastric acid secretion and, presumably, with an adequate mucosal blood flow reserve.
The gastric juice pH and tonometric PrCO2 were measured in 14 human volunteers, after gastric acid secretion suppression by either ranitidine (100-mg bolus, followed by 25 mg/h i.v., n = 7) or by ranitidine plus pirenzepine (10-mg bolus, followed by 3 mg/h i.v., n=7) to suppress any residual meal-stimulated gastric acid secretion, before and at 30-minute intervals until 120 minutes after oral ingestion of a standard liquid test meal (Pulmocare [Abbott, the Netherlands]; 500 mL, 750 kcal, P(CO2) 5 mm Hg, pH 7.50).
The gastric juice pH, which was >4.0 in all individuals throughout the study, and the PrCO2 did not depend on the regimen for gastric acid secretion suppression, and therefore the data were pooled. The PrCO2 (median [range]) after feeding was 69% (56% to 170%) of baseline (42 [37-51] mm Hg) from 0 to 30 minutes (P < .001), 85% (72% to 167%) of baseline from 30 to 60 (P < .05), 97% (57% to 193%) from 60 to 90 minutes, and 112% (97% to 189%) of baseline from 90 to 120 minutes with a rise above baseline in 10 of 14 patients. In vitro, the liquid test meal generated CO2 after adding bicarbonate but not after hydrochloric acid.
We recommend intragastric tonometry to be performed in the fasting state and discourage tonometry after feeding as a stress test, because a single test meal changes tonometric PrCO2 in a time-dependent manner until 2 hours after gastric feeding of healthy volunteers. The fall in PrCO2 directly after feeding can be attributed to dilution, whereas a rise above baseline in some patients may have been caused, as supported by CO2 production after adding bicarbonate to the test meal in vitro, by CO2 production through buffering of meal-derived acid by gastric bicarbonate, in the absence of stimulated gastric acid secretion by feeding.
如果抑制胃酸分泌以避免胃内二氧化碳通过胃内碳酸氢盐缓冲酸生成，通过眼压测量法检测反映黏膜内二氧化碳分压升高的高胃内局部二氧化碳分压（PrCO2），有助于诊断黏膜缺血。建议在禁食状态下进行眼压测量，但这可能会妨碍重症患者的喂养。另一方面，餐后眼压测量可作为一种诊断性应激试验，因为进食会增加黏膜血流需求，前提是餐食本身不妨碍二氧化碳从黏膜扩散到眼压测量球囊，且不产生胃内二氧化碳，与黏膜内二氧化碳分压无关。因此，我们研究了标准餐对健康志愿者胃内PrCO2眼压测量的影响，这些志愿者的餐食刺激胃酸分泌受到抑制，且可能具有足够的黏膜血流储备。
在14名人类志愿者中，通过雷尼替丁（100mg推注，随后以25mg/h静脉输注，n = 7）或雷尼替丁加哌仑西平（10mg推注，随后以3mg/h静脉输注，n = 7）抑制胃酸分泌，以抑制任何残留的餐食刺激胃酸分泌，在口服标准液体试验餐（Pulmocare[荷兰雅培公司]；500mL，750千卡，二氧化碳分压5mmHg，pH 7.50）之前及之后每隔30分钟测量胃液pH值和眼压测量的PrCO2，直至120分钟。
在整个研究过程中，所有个体的胃液pH值均>4.0，PrCO2不依赖于胃酸分泌抑制方案，因此将数据合并。进食后PrCO2（中位数[范围]）在0至30分钟为基线值（42[37 - 51]mmHg）的69%（56%至170%）（P <.001），30至60分钟为基线值的85%（72%至167%）（P <.05），60至90分钟为97%（57%至193%），90至120分钟为基线值的112%（97%至189%），14名患者中有10名患者的PrCO2高于基线值。在体外，加入碳酸氢盐后液体试验餐产生二氧化碳，但加入盐酸后不产生。
我们建议在禁食状态下进行胃内眼压测量，不建议将餐后眼压测量作为应激试验，因为在健康志愿者胃内喂食后2小时内，单一试验餐会以时间依赖性方式改变眼压测量的PrCO2。进食后PrCO2的下降可归因于稀释，而一些患者高于基线值的升高可能是由于体外试验餐中加入碳酸氢盐后产生二氧化碳，以及在无进食刺激胃酸分泌的情况下，胃内碳酸氢盐缓冲餐食衍生酸产生二氧化碳所致。
