Role of nitric oxide in apoptosis and cell necrosis for intestinal transplantation.

INTRODUCTION

Nitric oxide (NO) is an important mediator of both physiological and pathological responses. Its dual role in the ischemia-reperfusion syndrome is still a matter of controversy. The aim of this study was to analyze the effect of NO on apoptosis and cell necrosis associated with heterotopic small bowel transplant.

METHODS

Sprague-Dawley rats underwent heterotopic small bowel transplants with 3 hours of cold ischemia and 5 hours of reperfusion. Animals were assigned to the following study groups: Sham; bowel transplant (Trp); bowel transplant + NO donor (Trp + NONOS); bowel transplant + NO synthesis inhibitor (Trp + L-NAME). We studied histological changes and bacterial translocation in mesenteric nodes, liver and spleen as parameters of cell necrosis and caspase-3 activity as a parameter of apoptosis.

RESULTS

Histological changes and bacterial translocation showed that exogenous administration of NO protected the transplant. Simple bowel transplant, with or without inhibition of NO synthesis, did not display this protective effect. Significantly greater levels of apoptosis were observe in grafts among the group administered NO at pharmacological doses.

CONCLUSIONS

In experimental bowel transplantation rats administered exogenous NO show less necrosis but at the same time stimulation of apoptosis.