The administration of BCAA produces a significant increase in basal ventilation and CO2 response in adult humans and significant decrease in apneic episodes in premature infants. In order to assess the effect of BCAA on the neonatal ventilatory response to hypoxia, 13 sedated and spontaneously breathing piglets £7 days old were studied before and after a 4 hour infusion of 53% BCAA (n = 8) or 5% dextrose (D5W; n =5) solution. Minute ventilation (VdotE), oxygen consumption (VdotO2), arterial blood pressure (ABP), heart rate (HR), and arterial blood gases were measured in room air (RA) and during 1, 5 and 10 min of hypoxia (FiO2 = 0.10). Mean ± SD of absolute values and% change (Δ) from RA for VdotE (ml/kg/min) were as follows: Table Although a similar increase in VdotE occurred at 1 min of hypoxia pre- and post-BCAA, a significant increase in the ventilatory response at 5 and 10 min of hypoxia was noted post-BCAA. A significant increase in respiratory rate(p<0.002) and decrease in PaCO2 (p<0.004) were also observed after BCAA infusion. Changes in VdotO2, ABP, HR, pH, PaO2 and base excess with hypoxia were not different between pre- and post- BCAA. In the control group, the cardiorespiratory response to hypoxia was not modified by D5W infusion. These data suggest that the administration of BCAA increases central respiratory output and eliminates the ventilatory depression observed during sustained hypoxia in the neonate.

Table 1