GLUTATHIONE AND NITRIC-OXIDE CONCENTRATIONS IN GLUTAMINE-INFUSED RABBITS WITH INTESTINAL ISCHAEMIA REPERFUSION/

Intestinal ischaemia/reperfusion causes formation of reactive oxygen i ntermediates which lead to mucosal cell injury. Glutathione, a scaveng er of reactive oxygen intermediates, protects tissues from reactive ox ygen intermediate-mediate cell injury. Nitric oxide is a lipophilic ga s and its synthesis is stimulated by ischaemic conditions. In this exp erimental study, we aimed to investigate the role of i.v. L-glutamine infusion on mucosal tissue glutathione and serum nitric oxide concentr ations in intestinal ischaemia/reperfusion. External jugular vein of a lbino rabbits was cannulated with catheter and infused with normal sal ine at 4 ml/h. After 3 days, they were randomly divided into two main groups. Group 1 (n = 30) received i.v. normal saline alone, group 2 (n = 30) received normal saline + 205 mmol/l glutamine at 4 ml/h for 24 hours. Next, mucosal glutathione and serum nitric oxide concentrations were measured after 0, 30, 60 min of ischaemia/60 min of reperfusion. Basal glutathione concentrations were similar in normal saline alone and normal saline + 205 mmol/l glutamine infusion groups (p > 0.05). A t 30 and 60 min of ischaemia/60 min of reperfusion, glutathione concen trations were significantly lower in normal saline-infused rabbits com pared to the normal saline + 205 mmol/l glutamine-infused rabbits (p < 0.05). In addition, serum nitric oxide concentrations were found to b e significantly increased in rabbits 30 and 60 min after ischaemia/rep erfusion when compared to mean basal nitric oxide concentrations obtai ned from control animals. However, the normal saline + 205 mmol/l glut amine group had lower serum nitric oxide concentrations than did the n ormal saline alone group. In conclusion, this study revealed that inte stinal mucosal glutathione concentrations were significantly higher in glutamine-receiving rabbits than in non-receiving ones. Additionally, it was shown that nitric oxide concentrations increased in ischaemia both in normal saline alone and normal saline + 205 mmol/l glutamine r eceiving groups, while this increase in nitric oxide was more prominen t in the normal saline alone group (p < 0.01). These findings show tha t glutamine supplementation may protect the small intestine from ischa emia/reperfusion injury and may play a regulatory role in the biosynth esis of nitric oxide.