Abstract:
Background: Purulent-destructive lung diseases remain a priority among the causes of generalized infection and death. The
key to the progression of infection in acute lung abscesses may be associated with impaired barrier-filtration function of this
organ, which is based on endothelial dysfunction.
Methods: The experiments were carried out on 32 Chinchilla rabbits, in which the model of acute lung abscess was repro duced. Investigated in blood samples at the entrance and exit from the lungs, such indicators as nitrates, nitrites, peroxyni trite, NO-synthase and von Will brand factor.
Conclusion: Nitric oxide produced because of iNOS activation is intended for non-specific protection of the body against a
wide range of pathogenic agents, inhibits platelet aggregation and improves local blood circulation. However, these changes
do not occur. The main role in this direction is assigned to peroxynitrite, which, due to its pathogenicity, worsens the already
process associated with endothelial dysfunction. The nature of the changes in the parameters of the nitroxidergic regulation
of the endothelial system in the lungs has a staging: compensated and decompensated.
