Measurement of gastric wall PCO2 has emerged as a promising monitor of
perfusion deficits during low-flow states of circulatory shock. In th
e present study, gastric luminal PCO2 measured with the gastric tonome
ter was compared with the PCO2, measured directly in the wall of the s
tomach during hemorrhagic shock in two groups of five Sprague-Dawley r
ats. One group was pretreated with the H-2 blocker, ranitidine. During
a 120-min interval of hemorrhage, tonometer PCO2 increased from 60 +/
- 7 mmHg to 90 +/- 10 mmHg, and time-coincident gastric wall PCO2 from
52 +/- 5 mmHg to 131 +/- 14 mmHg. Following reinfusion of shed blood,
tonometer PCO2 remained elevated for an interval exceeding 60 min, bu
t gastric wall PCO2 returned to control levels within approximately 10
min. Ranitidine pretreatment did not alter the relationships between
gastric wall PCO2 and tonometer PCO2. These observations indicate that
gastric luminal PCO2 underestimates relatively rapid increases in gas
tric wall PCO2 during profound hemorrhagic shock in rats. (C) 1993 Wil
ey-Liss, Inc.