In patients with septic shock an iloprost-induced increase in cardiac index increased splanchnic blood flow and shifted oxygen utilization from the energy requiring de novo glucose production rate to other oxygen-demanding metabolic pathways.

In 12 patients with hyperdynamic septic shock we studied the effect of dopexamine, a combined dopamine and beta-adrenergic agonist, on hepatosplanchnic hemodynamics and O(2) exchange. All patients required noradrenaline to maintain mean arterial pressure > 60 mm Hg (noradrenaline >/= 0.04 microg x kg(-1) x min(-1)) with a cardiac index >/= 3.0 L/min/m(2). Splanchnic blood flow (Qspl) was measured using primed continuous infusion of indocyanine green dye with hepatic venous sampling. In addition tonometric gastric mucosal-arterial and gastric mucosal-hepatic venous P CO(2) gradients were assessed as indicators of regional energy balance. After 90 min of stable hemodynamics a first measurement was obtained. Then dopexamine infusion was titrated (1-4 microg x kg(-1) x min(-1)) to increase cardiac output by approximately 25% (20-30%). After 90 min all measurements were repeated, and dopexamine was withdrawn followed by a third measurement. Median Qspl (0.86/1.23-0. 66 versus 0.96/1.42-0.85 L/min/m (2) [median value/25th-75th percentiles], p < 0.05) increased whereas the fractional contribution of Qspl to total blood flow decreased (21/28-13 versus 19/28-12%, p < 0.05). Although both global and regional oxygen delivery (DO(2)) consistently increased, neither global or regional V O(2) nor PCO(2) gradients were significantly affected. In patients with septic shock and ongoing noradrenaline treatment dopexamine seems to have no preferential effects on hepatosplanchnic hemodynamics, O(2) exchange, or energy balance.

To determine the influence of changes in gastric juice pH due to intravenous administration of pentagastrin and omeprazole on intramucosal regional PCO2 (Pr(CO2)), we investigated 17 healthy human volunteers. Gastric juice pH was obtained from a glass pH electrode for continuous gastric juice pH measurement and Pr(CO2))was measured by using automated air tonometry. After baseline (8:00 A.M.-9:00 A.M.) the subjects received 0.6 microg/kg/h pentagastrin intravenously for 1 h (9:00 A.M.-10:00 A.M., after stimulation 10:00 A.M.-11:00 A.M.) and 40 mg omeprazole intravenously (after omeprazole 11:00 A.M.-3:00 P.M.). Following pentagastrin administration gastric juice pH significantly decreased from 1.2 +/- 0.4 to 0.6 +/- 0.4 (mean +/- SD, p < 0.007, versus baseline), whereas omeprazole transiently increased luminal pH up to 4.4 +/- 1.7 (p < 0.007 versus baseline). These subsequent changes in gastric juice pH were accompanied by a significant increase in Pr(CO2) from 48 +/- 12 to 61 +/- 17 mm Hg (p < 0.007 versus baseline) and a decrease to 44 +/- 5 mm Hg (p < 0.002 versus pentagastrin), respectively. A gastric juice pH > 4 considerably reduces mean gastric Pr(CO2) and interindividual variability. Thus omeprazole may improve the validity of gastric tonometry data.

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Background: Gastric regional CO₂ accumulation indicates gastric mucosal hypoperfusion in critically ill patients. CO₂ is also a reaction product of urea degradation, and we therefore tested the hypothesis if regional pCO₂ is influenced by Helicobacter pylori infection. Material: Seven H. pylori-positive and 7 H. pylori-negative volunteers (age range 21–30 years) were investigated. During a 6- to 7-hour observation period, we obtained every 30 min arterial blood gases, gastric juice pH from a glass pH electrode and regional pCO2 from a gastric tonometer. The study protocol included subsequent periods of baseline measurements, pentagastrin stimulation (0.6 µg/kg/h/i.v.) and application of omeprazole (40 mg i.v.). Results: Gastric regional pCO₂ was increased in H. pylori-positive versus H. pylori-negative subjects before (64.4 ± 3.1 vs. 50.0 ± 2.9 mm Hg, p < 0.005) but not after application of omeprazole. The effect of omeprazole on gastric juice pH was increased in H. pylori-positive subjects (mean pH during 4 h 6.1 ± 0.3 in H. pylori-positive vs. 2.5 ± 0.2 in H. pylori-negative subjects; p < 0.0001). There was a difference in arterial pCO₂ between H. pylori-positive and H. pylori- negative subjects (43.1 ± 0.3 versus 38.9 ± 0.3 mm Hg; p < 0.0001). Conclusion:H. pylori infection has a significant effect on gastric regional CO₂ that is suppressed by application of a proton pump inhibitor.