The purpose of this study was to analyze the
nicotinamide adenine dinucleotide phosphate -
diaphorase (NADPH-d) activity in the rat jejunum after a
mesenteric ischemia/
reperfusion injury.
Nitric oxide, synthetised from
L-arginine by the
enzyme nitric oxide synthase, is a nonadrenergic noncholinergic relaxant
neurotransmitter of the intestinal smooth muscle. It plays an important role in the process of plasticity after the
ischemia/reperfusion injury. Experimental animals were divided in two groups: the control group and the ischemic/reperfusion group, with different period of the reperfusion. The
NADPH-d histochemical method has been used as a marker for the
nitric oxide synthase.
NADPH-d activity has been rapidly decreased in the neurons of both enteric nervous systems in plexuses of the jejunum after 1 h
mesenteric ischemia and 1 h reperfusion. Differences were predominantly detected in the myenteric plexus; they were seen in change of the neuronal shape, in the arrangement of neurons and in intensity of their staining. The
NADPH-d positivity was absent in the intestinal crypts. After 1 h
ischemia and 24 h reperfusion, the
NADPH-d activity was gradually increased, but it was lower in comparison with the control group. On the 30th day following the
ischemia/reperfusion there were no changes in
NADPH-d positivity compared with the control animals. These results indicated that the jejunal
ischemia/reperfusion has affected the neurons of the enteric nervous system of adult rats and resulted in the early decrease of
NADPH-d positivity 1 h of the reperfusion insult. The gradual increasing of
NADPH-d activity in 24 h following the reperfusion could be considered as a result of the plasticity process. On the 30(th) day after the
ischemia/reperfusion all histochemical changes were returned to the control levels.