GASTRIC INTRAMURAL PCO2, AS MONITOR OF PERFUSION FAILURE DURING HEMORRHAGIC AND ANAPHYLACTIC SHOCK

Indirect measurement of gastric intramural pH (pH(G)) utilizing a lumi nal tonometer in the stomach has been proposed for monitoring the seve rity and progression of perfusion failure. In the present study, we in vestigated gastric Pco(2) and pH(G) as indicators and quantitators of the severity of perfusion failure in the experimental rodent model of both hemorrhagic and anaphylactic shock. Gastric intramural Pco(2) (PG (co2)) and PHG were directly measured with miniaturized sensors insert ed into the anterior wall of the stomach. In hemorrhagic shock, animal s were bled into a reservoir maintained at a pressure of 35 mmHg. pH(G ) decreased from 7.39 +/- 0.08 to 6.67 +/- 0.11 (P < 0.01), and PG(co2 ) increased from 53 +/- 4 to 136 +/- 3 Torr (P < 0.01). Anaphylactic s hock was induced in animals that had been sensitized 21 days before wi th crystallized ovalbumin. Antigen challenge produced an immediate red uction in mean aortic pressure from 144 to 60 mmHg. pHG decreased from 7.40 +/- 0.05 to 6.99 +/- 0.07 (P ( 0.01), and PG(co2) increased from 48 +/- 5 to 133 +/- 9 Torr (P ( 0.01). The increases in PG(co2) were highly correlated with decreases in gastric blood flow in both hemorrh agic (r = 0.96) and anaphylactic shock (r = 0.92). The correlations wi th pH(G) were more moderate. These experiments demonstrated prominent increases in PG(co2) and H+ during both hemorrhagic and anaphylactic s hock. We further noted that the estimation of pH(G) based on the assum ption that HCO3- concentrations of the stomach wall and arterial blood are the same was not fully sustained.