Intramucosal pH changes following complete segmental small intestinal ischemia, as compared with the effects of superior mesenteric artery occlusion.

Microcirculatory nonperfusion of the intestinal mucosa may result in a subsequent prolongation of tissue ischemia, even after restoration of the mesenteric blood flow. It was hypothesized that there is a relationship between mucosal no-reflow and the amount of previously ischemic tissues during intestinal ischemia reperfusion. Accordingly, an examination was made of the changes in intestinal and gastric intramucosal pH (pHi) in dogs after a 120-min complete occlusion of the superior mesenteric artery (SMA) and those observed following ischemia of an ileal segment only. pHi, as an indicator of the adequacy of mucosal microcirculatory perfusion, was calculated by the tonometer technique. Baseline values of intestinal pHi (mean 7.25 +/- 0.12) and gastric pHi (mean 7.23 +/- 0.27) were determined in sham-operated animals. The 120-min intestinal ischemia caused a progressive fall in intestinal pHi to a mean value of approximately 6.8. Reperfusion resulted in a slow return to nearly normal pHi levels in the ileal segment, but essentially no intestinal pHi elevation was observed during the 90-min period following occlusion of the SMA. The gastric pHi remained at the control level during segmental intestinal ischemia reperfusion, but declined below the normal range following release of the occlusion of the SMA. It is proposed that continuing microcirculatory nonperfusion could explain the failure to demonstrate a postreperfusion elevation of pHi following complete occlusion of the SMA.