Decrease in mucosal alkaline phosphatase: A potential marker of intestinalreperfusion injury

Intestinal ischemia necessitates rapid re-establishment of blood flow to pr event irreversible anoxic tissue damage. However, reperfusion results in ad ditional injury as a consequence of the generation of oxygen free radicals. To date, no clear-cut marker to differentiate between ischemia versus repe rfusion injury is available. In this regard, previous studies from our labo ratory utilizing a rat in vitro lipid peroxidation model demonstrated that the generation of free radicals resulted in the inactivation of only the in testinal brush border alkaline phosphatase enzyme, with no effect on other membrane-bound digestive enzymes, Current studies were designed to assess t he possibility of alkaline phosphatase being a specific marker of the reper fusion injury in canine and human ex vivo ischemia/reperfusion models. Smal l bowels harvested from canines and organ donors were subjected to ischemia followed by reperfusion, Brush border membrane enzymes, alkaline phosphata se, sucrase, maltase, and gamma-glutamyl transpeptidase were assayed in muc osal extracts from intestines with ischemia versus reperfusion. In both exp erimental models, there was no change in any enzyme activity with warm isch emia alone. In contrast, alkaline phosphatase activity was significantly de creased in both the canine and human reperfusion models, with no change in specific activities of sucrase, maltase, and gamma-glutamyl transpeptidase, Our data indicate that the alkaline phosphatase enzyme activity may repres ent a potential marker of intestinal reperfusion injury and may permit quan titative assessments of therapeutic interventions in human intestinal reper fusion injury.