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Experimental Surgery

The Prophylactic Effect of L-arginine in Acute Ischaemic Colitis in a Rat Model of Ischaemia/reperfusion Injury

, , , , , , , , , & show all
Pages 192-200 | Published online: 11 Mar 2016
 

Abstract

Background/Aims: The decreased synthesis of nitric oxide (NO) during ischaemia/reperfusion (I/R) has been implicated as the major underlying mechanism for the pathogenesis of acute ischaemic colitis (A.I.C.). The aim of this study was to investigate the prophylactic effect of L-arginine, a NO donor, on tissue injury during intestinal I/R, and compare its efficacy with that of exogenous vasodilators (molsidomine) and inert nitrogen-containing molecules (casein). Material and methods: One hundred forty four Wistar rats underwent occlusion of the superior mesentery artery for 30, 60 and 90 min for induction of intestinal ischaemia, followed by 90 min of reperfusion. The rats were randomly assigned to receive L-arginine, molsidomine, or casein hydrolysate. In all groups, apart of the histological study, we determined the levels of serum malondialdehyde (MDA), a reliable marker indicating the degree of the tissue damage after intestinal I/R. Results: Serum MDA levels were significantly lower in the L-arginine group compared to the untreated animals or those that had received molsidomine or casein, after a period of ischaemia of 90 minutes (p < 0.0005), as well as after a period of ischaemia of 60 or 90 minutes followed by a 90 minutes reperfusion (p = 0.011, and p < 0.0005, respectively). In addition, lesser histopathological damage was noted after the use of L-arginine compared to that caused by the administration of molsidomine and casein.

Conclusion: These findings support a prophylactic effect of L-arginine in experimentally induced intestinal ischaemia. In short, L-arginine attenuates the degree of tissue damage in intestinal ischaemia and promotes healing of intestinal mucosa.

Additional information

Notes on contributors

M. Genetzakis

M. Genetzakis 31 Kononos Str GR-11634 Athens, Greece Tel.: +30 210 7217951 Fax: +30 210 7217951 E-mail: [email protected]

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