Organ specific formation of nitrosyl complexes under intestinal ischemia/reperfusion in rats involves nos-independent mechanism(s)

Intestinal ischemia/reperfusion may lead to local and distant organ damage involving nitric oxide (NO). NO rapidly reacts with heme/non-heme-iron-yiel ding nitrosyl complexes, which can be determined directly by electron param agnetic resonance spectroscopy. The aim of the present study was to charact erize nitrosylation reactions induced by transient intestinal ischemia in b lood and tissues. We used electron paramagnetic resonance spectroscopy and reverse transcription polymerase chain reaction analyses to estimate nitros yl complex levels and inducible NO synthase mRNA expression in rats subject ed to superior mesenteric artery occlusion for 60 min followed by the reper fusion. Nitrosyl hemoglobin concentrations in circulating blood were signif icantly increased during ischemia and reperfusion. Nitrosyl hemoglobin comp lexes were detected in ischemic intestine, but not in normoxic lung and liv er or reperfused intestine. Administration of N-G-monomethyl-L-arginine, a non-specific NO synthase inhibitor, did not affect the formation of circula ting nitrosyl complexes. Moreover, inducible NO synthase mRNA was not found in intestinal tissues at 30 min of reperfusion. Our data suggest an organ- specific NO formation indicated by the increased nitrosylation reaction in ischemic intestinal tissue, but not in the distant normoxic organs, in spit e of high circulating nitrosyl hemoglobin levels. NO involved in nitrosylat ion under intestinal ischemia/reperfusion is probably formed by NO synthase -independent mechanism(s).