Features of the Response of the Respiratory Center of Newborn Rats That Were Exposed to Prenantal Passive Smoking to Hypoxia (In Vitro)

It is expected that in neonates that underwent prenatal chronic effect of nicotine the identification of the reduction of intensiveness of respiratory response to hypoxic exposure may be the cause of sudden infant death. The effect of cigarette smoke may differ from the effect of nicotine. The study was performed on brain stem spinal cord preparations (BSS) in the brain of newborn rats (n=38) in vitro. In the experimental group (EG) the modeling of passive smoking was carried out by fumigation of cigarette smoke of rat females from the 1st to 20th day of gestation. Hypoxia was simulated by an artificial cerebrospinal fluid saturated with a gas mixture of 5% CO2 and 95% N2. Hypoxic depression of BSS respiratory rhythm of the control group (CG) occurred at the 5th minute; the restoration took place in 10 minutes at normoxia, at the same time there was an increase of the amplitude of the inspiratory discharges which did not return to baseline values (15 minutes). In preparations of CG at the 10th minute of hypoxia the duration of inspiratory discharges decreased and restored after 10 minutes at normoxia. The increase of the ratio of the power of low-frequency and medium-frequency oscillations was observed in the CG at the 15th minute of hypoxia with the restoration during 10 minutes. In the experimental group (EG) the increase of the duration of the respiratory cycle occurred at the 10th minute of hypoxia with the dynamics of recovery similar to that of CG. The increase of the amplitude of inspiratory discharges occurred at the 10th minute of hypoxia; a recovery period took 10 minutes. In the BSS of EG the reduction in the duration of the inspiratory discharges and the increase of the ratio of the power oscillations of low- and mid-range occurred at the 5th and 10th minutes of hypoxia and these parameters never returned to baseline values. Our data suggest that prenatal exposure to secondhand smoke has an effect on the mechanisms of central chemosensitivity in the offspring in the early postnatal period.