[Disorder of the serum albumin transport function in chronic oxygen starvation and its pharmacological correction].

Grade II chronic intermittent hypoxic hypoxia under normal barometric pressure, which was reproduced in pregnant rats 2.0-2.5 weeks before expected delivery and in the offsprings in the first 2 days of neonatality caused a decrease in serum albumin functional activity associated with bilirubin transport, as evidenced in vitro, as well as accumulation of serum albumin-bound nonesterified higher fatty acids and acetaldehyde along with uncompensated acidosis, an increase in brain levels of bilirubin in adult and newborn rats, and enhancement of its hemoxygenase activity. Administration of alpha-tocopherol acetate, nicotinamide, sodium oxybutyrate, and trisamine to animals exposed to hypoxia normalized the above biochemical parameters, except for hemoxygenase activity and promoted a greater binding of endogenous bilirubin to albumin in adult and newborn rats in vivo.