Prenatal cocaine alters normoxic sleep-wake and diaphragmatic EMG patterns in piglets.

This study assessed in piglets the effects of prenatal cocaine administration on sleep-wake states (SWS) and respiratory parameters, utilizing diaphragmatic electromyogram (EMGdi) recordings during normoxia before and after hypoxia (0.10 F(I,O2), 10 min). We asked whether the respiratory effects were linked to a specific SWS, and whether there was a difference in respiratory measures between the two normoxic conditions. Unsedated, chronically instrumented 3-9- or 21-31-day-old piglets, representing distinct stages in developmental respiratory control, were used. In pre-hypoxic normoxia, prenatal cocaine enhanced sleep at the expense of wakefulness and increased EMGdi amplitude, slope, and area in both age groups regardless of SWS; after the hypoxia, the respiratory findings persisted in the young group, but disappeared in the older group [corrected]. In the young group and regardless of SWS, interbreath interval (ttot) and expiratory duration (ttot - tEMGdi[duration of EMGdi]) were shorter in the cocaine-exposed than in the unexposed piglets, and ttot, tEMGdi, and (ttot - tEMGdi) decreased from pre- to post-hypoxic normoxia. In the older group, ttot and (ttot - tEMGdi) differed among SWS, but were unaffected by drug treatment; tEMGdi was higher with cocaine exposure in pre-, but not in post-hypoxic normoxia, and two-thirds of the EMGdi measurements during post-hypoxic normoxia exhibited a similar magnitude in the drug-treated and untreated groups regardless of SWS. We conclude that 1) prenatal cocaine alters both SWS and EMGdi, but the EMGdi effects are independent of SWS; and 2) the similar EMGdi patterns in the older group after hypoxia, regardless of drug treatment, suggest that hypoxia and chronic prenatal cocaine might alter EMGdi by similar mechanisms.