THE ROLE OF ANTITIPOXANS IN CORRECTING ACID BASE STATE IN THE BLOOD IN INFANTS BORN WITH CHRONIC HYPOXIA

The primary cause of hypoxic-ischemic brain injury is widely recognized as the restriction of both oxygen supply and essential oxidative substrates necessary for cellular function. This understanding is supported by existing research ([3,4]). The most critical damage to brain cells occurs 2-6-48 hours after birth due to oxidative stress. This process is triggered by the resumption of blood flow to the brain following a period of oxygen deprivation (perfusion deficit). The reintroduction of highly oxygenated blood leads to an overproduction of harmful free radicals, contributing to cell damage. A study involving 60 premature infants who experienced asphyxia during birth was conducted at the Samarkand Regional Perinatal Centre and the Neonatal Intensive Care Unit of the Samarkand Multidisciplinary Children's Research Medical Centre. These infants were closely monitored to observe the effects of oxidative stress on brain tissue. Key words: asphyxia, newborns, cerebroprotector, Cytoflavin