Bioenergy metabolism of gastric mucosa during stress

Previous studies have identified a cellular energy deficit in gastric mucosa after ischemia. We studied the processes of energy generation (mitochondrial function) and energy utilization (microsomal adenosine triphosphatase [ATPase] activity) in an experimental model of stress. Rabbits were divided into four groups: I, fed controls (n = 7); II, 24-hour fasted controls (n = 7); III, fasted, anesthetized, and cannulated controls (n = 7); and IV, fasted, anesthetized, cannulated, and bled rabbits. Bleeding consisted of 25 ml blood/kg into a reservoir for 60 minutes; the blood was then reinfused. Animals were killed 30 minutes after reinfusion; antral, corpus, and fundus mucosae were dissected; each region of mucosa was homogenized; and mitochondrial and microsomal fractions were isolated by differential centrifugation. No animals in group I or II had gastric ulcerations. Three of seven animals in group III and all group IV animals had corpus and fundus ulcers. No antral ulcers were seen in any group. The respiratory control index (RCI) of antral mitochondria was increased in groups II, III, and IV but was unchanged in all groups of corpus and fundus mitochondria. Studies of microsomal ATPase activity indicated increased activity of potassium-stimulated ATPase in the corpus mucosa. In the corpus mucosa, total ATPase activity was increased primarily as a consequence of increased potassium-stimulated ATPase. These data indicate that increased RCI is associated with gastric mucosal integrity in the antrum. Accelerated utilization of available adenosine triphosphate by corpus membrane ATPases may further compromise energy homeostasis during stress.