Hypoxoco-ischemic changes in bronchopulmonary dysplasia in premature children

Abstract

Pulmonary pathology in children born prematurely, during infancy, is characterized by the peculiarities of nosological forms. Understanding and deciphering some pathogenetic mechanisms that contribute to the maintenance of hypoxia is extremely relevant [16].Material and methods. The principle of the modified ischemic albumin dosing method is based on the property of albumins to bind Co2+ ions, which determines the decrease in the color intensity of the solution, which is measured photometrically at 492 nm [23].Results. The analysis of the obtained results reveals a lower hemoglobin oxygen saturation in children with bronchopulmonary dysplasia compared to healthy children (by 2%, p=0.031), the differences being statistically true. The extent of the decrease is not major, but the data revealing cellular oxidative tendencies attest to a lack of oxygen compared to the needs of the cell. Conditions of hypoxia, ischemia, acidosis, as well as the exacerbation of free radical production cause the degradation of the N-terminal region of serum albumin with the formation of ischemic modified albumin (MIA). In our study, a statistically significantly higher level of serum AIM was recorded in children with bronchopulmonary dysplasia (by 74%, p<0.001) compared to the values identified in children without DBP. Conclusions: In children with bronchopulmonary dysplasia, tissue hypoxic lesions can be evaluated by significantly increased MIA values, and their detection in chronic respiratory conditions is considered a useful diagnostic test.