No abstract

Changes in O2 consumption, O2 extraction, and intramural pH, resulting from a decreasing O2 delivery, were studied in the intact dog intestine. The O2 delivery was decreased by ischemia, hypoxia, and combined hypoxia-ischemia. A noninvasive approach for determining intramural pH based on the principle of tonometry was used. There was a strong correlation between the changes in intramural pH and intestinal O2 consumption as O2 delivery was decreased. Intramural pH and O2 consumption were initially maintained in the face of decreasing O2 delivery, but after a critical point they decreased. This critical point was 60.3 +/- 1.6% of base-line O2 delivery in the ischemic group and 51.3 +/- 2.7% of base line in the hypoxic-ischemic group. Despite a decrease to 36.0 +/- 5.6% of base-line O2 delivery, the intramural pH and O2 consumption did not decrease in the hypoxic group. O2 extraction increased with decreasing O2 delivery but did not plateau, indicating no diffusion limitation. The data suggest that blood flow is the major factor limiting intestinal O2 consumption. It is concluded that the noninvasive measure of intramural pH is a good marker of the adequacy of tissue oxygenation in canine intestine.

No abstract

We have examined the back-diffusion of CO2 generated by buffering HCI with NaHCO, in the stomach, observed its influence on the pH in the wall of the gastric mucosa, and compared its effects with those of HCl. Isolated stomachs of 17 anesthetized dogs were exposed to either (I) 250 ml NaCl at pH 7, or (2) 125 ml HCl (12.5 meq) + 125 ml NaHCO, (12.5 meq) to generate 12.5 meq CO2 in the stomach, or (3) 250 ml HCI alone to give either 12.5 or 35 meq HCl in the stomach. Samples of gastric fluid and arterial blood were collected every 20 min for 6 hr and analyzed for pH and pC02. The intramural pH of the gastric wall was measured by hollow viscus tonometry. The pC02 in gastric juice rose to 1184 + 139 mm Hg upon the generation of CO2 in the stomach. The till of the CO2 generated by the buffering of acid was 32 + 4 min and of the pC02 was 18.7 f 0.7 min. The till of an equimolar amount of HCI was 2 hr 42 min f 40 min. The disappearance of the CO, was accompanied by a rise in intragastric pH from 6.0 f 0.01 to 6.8 + 0.09 (P < 0.05). and by a fall in intramural pH in the gastric wall from control values of 7.31 + 0.05 to 6.3 f 0.8 (P .Z 0.001). In contrast the pH in gastric fluid did not change and the pH in the intramural fluid did not fall below control values following the administration of 12.5 or 35 meq HCI alone.

No abstract