Nitrergic innervation of small intestine in rats after ischemic-reperfusion injury
Adriana Boleková Orcid.org 1, Tatiana Špakovská Orcid.org 1, Darina Kluchová Orcid.org 1, Štefan Tóth Orcid.org 2, Jarmila Veselá Orcid.org 2
1 Ústav anatómie LF UPJŠ v Košiciach
2 Ústav histológie a embryológie LF UPJŠ v Košiciach
Even nowadays, multiple organ failure syndrome still causes high mortality, therefore it needs special attention. Endothel of the small intestine causes bacterial translocation as well as local and systemic inflammation, the main pathophysiological changes that lead to the development of the syndrome. Nitric oxide is a nonadrenergic and noncholinergic neurotransmitter in the intestinal smooth muscle and it plays an important role in the process of ischemic-reperfusion injury.
Methods: Experimental animals, adult male Wistar rats, were divided into three groups according to the reperfusion period after previous ischemic episode lasting for one hour. The results were compared to a control group without experimental ischemic-reperfusion injury. Samples of the jejunum were histochemically analyzed in order to visualize the nicotinamide adenine dinucleotide phosphate diaphorase, which is a marker of the nitric oxide in the nerve structures.
Results: The activity of the nitrergic neurons rapidly decreased in the group with one hour reperfusion; consequently, this activity gradually increased in the group with 24 hour reperfusion, and finally in the group with 30 days reperfusion there were no changes in the activity of the nitrergic neurons compared to the control group.
Conclusion: These results indicated that the jejunal ischemic-reperfusion injury affected the neurons of the enteric nervous system and resulted in early decrease in the activity of the nitric oxide neurotransmitter one hourafterthe injury. Further gradual increase of its activity 24 hours after ischemic-reperfusion injury could be considered a result of the plasticity process. On day 30 after ischemic-reperfusion injury all the histochemical changes reached control levels. After the compensation mechanisms failure, death occurred within a week after elicited ischemia.
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