АДАПТИВНАЯ РОЛЬ ОКСИДА АЗОТА У НЕДОНОШЕННЫХ НОВОРОЖДЕННЫХ ДЕТЕЙ С ИШЕМИЕЙ МИОКАРДА В РАННЕМ НЕОНАТАЛЬНОМ ПЕРИОДЕ

Abstract

Objective of the study: to study the role of nitric oxide (NO) in adaptive reactions of the circulatory system in premature infants with transient myocardial ischemia (TMI). Materials and methods of research: a clinical, prospective, comparative study was carried out from 2016 to 2018. 82 infants with gestational age of 31–36 weeks who have had respiratory failure were included. Newborns were divided into groups: 1st – 14 newborns with TMI ECG criteria and troponin I (TrI) >0.139 ng/ml, 2nd – 39 newborns with TMI ECG criteria and TrI<0.139 ng/ml, 3rd – 29 children with normal ECG and TrI<0.139 ng/ml. In the early neonatal period, the clinical status, blood gas analysis, ECG, echocardiography and determination of TrI and NO were carried out. Quantitative data are presented as median, 25th and 75th percentiles; qualitative – in absolute values and %. The statistical significance was assessed by the Mann–Whitney test, the analysis of the relationship was assessed by the Spearman's rank correlation coefficient. Results: the level of NO by the 7th day of life in premature newborns of the 1st group increased 3.8 times, in the 2nd and 3rd groups – 1.7 and 2.5 times. A correlation relationship was revealed between TrI and NO on the 7th day of life (r=0.793, p=0.006), between NO and pH (r=–0.738, p=0.036), NO and pCO2 (r=0.857, p=0.006) on the 1st day. Also, on the 1st day there was a statistically significant increase in the end diastolic (EDS) and end systolic sizes (EDS) of the left ventricle (LV), the relationship of LV EDS with NO (r=0.722, p=0.042) and TrI (r=0.666, p=0.049), as well as NO with the LA size (r=0.731, p=0.038) in the 1st group. Conclusions: in premature infants with TMI and destructive changes in the myocardium, an increase in NO is probably necessary to optimize LV contractility and compensate for damage to cardiomyocytes. In children with TMI in the absence of myocardial injury, a compensatory increase in NO contributes to limiting the effects of hypoxia by functional disorders of LV, which persist by the end of the early neonatal period.