Faculty Bibliography

The effects of acute metabolic alkalosis and acidosis on intestinal electrolyte transport were studied in adult Sprague-Dawley rats. Animals were made alkalotic or acidotic by gavage feeding of 1 M solutions of NaCl (pH = 7.42), NaHCO3 (pH = 7.52), NH4Cl (pH = 7.18), or 0.75 M (NH4)2SO4 (pH = 7.21). After 1-3 h, animals were anesthetized and prepared for in vivo perfusion of the jejunum, ileum, and colon. The jejunum exhibited increased net potassium absorption in alkalosis and decreased potassium absorption in acidosis. In the ileum, net sodium absorption and potassium secretion were decreased, and bicarbonate secretion was increased in alkalosis, and opposite effects were observed in acidosis. The ileal lumen minus blood gradient for PCO2 (an index of hydrogen ion secretion) was greater in acidotic than in alkalotic animals. The levels of ileal sodium, bicarbonate, and potassium transport and the PCO2 gradient correlated well with the plasma pH and bicarbonate concentration in individual animals. In the colon, net bicarbonate secretion and chloride absorption increased and potassium secretion decreased in alkalosis, and opposite effects were observed in acidosis. The colonic lumen minus blood PCO2 gradient was not affected by acid-base balance. Colonic bicarbonate transport correlated with the plasma chloride concentration as well as with the plasma pH. The acid-base disorders had no effect on transmural potential difference. These results suggest that acute metabolic alkalosis and acidosis alter sodium and hydrogen ion transport in the ileum and chloride and bicarbonate transport in the colon

In spite of several macroscopic criteria for predicting the presence of histological abnormalities in rabbit ileum, microscopic ileal abnormalities still can escape detection. The effect of histologically abnormal rabbit ileum was evaluated on basal intestinal absorption, on basal absorption, on basal adenylate cyclase activity, and on cholera toxin-induced secretion and cholera toxin-induced stimulation of adenylate cyclase activity. Compared to histologically normal rabbit ileum, the presence of histological abnormalities was associated with decreased basal intestinal water, Na, Cl, and glucose absorption, absent glucose-dependent water absorption, and elevated basal adenylate cyclase activities. However, histologically abnormal rabbit ileum responded to inoculation of purified cholera toxin with stimulation of intestinal water secretion and adenylate cyclase activity similar to that in histologically normal ileum. These data have implications concerning the design of experiments that attempt to study the pathogenesis of diarrheal diseases by correlating changes in ileal transport with changes in ileal mucosal adenylate cyclase activity. In spite of abnormal ileal histology, studies of intestinal secretory states which attempt to define the role of adenylate cyclase in secretory processes can be performed provided animals are used as their own controls. However, when groups of animals are compared, the presence of an histologically abnormal ileum can cause changes in basal and intestinal secretagogue-stimulated ileal water and electrolyte transport and in basal and intestinal secretagogue-stimulated mucosal adenylate cyclase activity which can lead to erroneous conclusions if the presence of the abnormal ileal histology is not considered.