Ammonia excretion was studied in rat ileal segments during perfusion of the animal through the saphenous vein. In the first 10 min during and after intravenous infusion of L-glutamine (116 mg/ kg to double arterial glutamine concentration) average net change in lumenal ammonia was 13 ± 8 (S.E.) nmole NH3/min/g ileum; average net change in ileal venous ammonia was 28 ± 9 nmole NH3/min/g ileum; and average net change in total ammonia (lumen + ileal vein) was 41 ± 13 compared to —5 ± 10 nmole/ min/g ileum for animals infused with saline P < 0.025. These data suggest that ileal metabolism of arterial glutamine liberates am-monia to both ileal venous blood and intestinal lumen. When a cation-exchange resin which binds ammonia was infused intralu- menally, average net change in lumenal ammonia in the first 10 min during and after intravenous infusion of 116 mg/kg L-gluta- mine was 415 ± 156 nmole NH3/min/g ileum (p<0.01 compared to value during perfusion of Earle’s solution alone). During the first 10 min during and after glutamine infusion net change in ileal venous plasma ammonia was —8 ± 14 when resin was being perfused through the lumen compared to -1-28 ± 9 nmole/min/g ileum during perfusion of Earle’s solution alone without resin P < 0.05. Thus resin in the small intestine can trap very large amounts of ammonia. Speculation: Ammonia-binding cation-exchange resins may be useful therapeutically in lowering portal venous ammonia and increasing intestinal ammonia excretion in patients with hyperammonemia.