Glutathione and nitric oxide concentrations in glutamine-infused rabbits with intestinal ischaemia/reperfusion.
Intestinal ischaemia/reperfusion causes formation of reactive oxygen intermediates which lead to mucosal cell injury. Glutathione, a scavenger of reactive oxygen intermediates, protects tissues from reactive oxygen intermediate-mediated cell injury. Nitric oxide is a lipophilic gas and its synthesis is stimulated by ischaemic conditions. In this experimental study, we aimed to investigate the role of i. v. L-glutamine infusion on mucosal tissue glutathione and serum nitric oxide concentrations in intestinal ischaemia/reperfusion. External jugular vein of albino rabbits was cannulated with catheter and infused with normal saline 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). At 30 and 60 min of ischaemia/60 min of reperfusion, glutathione concentrations were significantly lower in normal saline-infused rabbits compared to the normal saline + 205 mmol/l glutamine-infused rabbits (p < 0.05). In addition, serum nitric oxide concentrations were found to be significantly increased in rabbits 30 and 60 min after ischaemia/reperfusion when compared to mean basal nitric oxide concentrations obtained from control animals. However, the normal saline + 205 mmol/l glutamine group had lower serum nitric oxide concentrations than did the normal saline alone group. In conclusion, this study revealed that intestinal 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 receiving groups, while this increase in nitric oxide was more prominent in the normal saline alone group (p < 0.01). These findings show that glutamine supplementation may protect the small intestine from ischaemia/reperfusion injury and may play a regulatory role in the biosynthesis of nitric oxide.
Başoğlu
M
M
Department of General Surgery, School of Medicine, Atatürk University Erzurum, Turkey.
Yildirgan
I
I
Akçay
F
F
Kiziltunç
A
A
Kavak
I
I
Oren
D
D
D000818:Animals; D016166:Free Radical Scavengers / Q000378:metabolism; D005973:Glutamine / Q000008:administration & dosage / Q000494:pharmacology; D005978:Glutathione / Q000378:metabolism*; D007262:Infusions, Intravenous; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism; D007421:Intestine, Small / Q000098:blood supply* / Q000293:injuries* / Q000378:metabolism; D008297:Male; D009569:Nitric Oxide / Q000097:blood*; D011817:Rabbits; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000378:metabolism* / Q000517:prevention & control
D016166:Free Radical Scavengers; D017382:Reactive Oxygen Species; D005973:Glutamine; D009569:Nitric Oxide; D005978:Glutathione