Abstract:
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.
Method: The experiments were carried out on 32 Chinchilla rabbits, in which the model of acute lung abscess was reproduced.
Investigated in blood samples at the entrance and exit from the lungs, such indicators as nitrates, nitrites, peroxynitrite,
NO-synthase and von Willebrand 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. All this is of a natural nature, based
on certain relationships between the indicators of the nitroxidergic regulation system
