Abstract

Intrauterine cocaine exposure causes subtle neurologic abnormalities in human newborn infants; however, the mechanism for these abnormalities is not known. To investigate whether cocaine alters fetal behavioral state, the electrocortical, electro-ocular and neck muscle electrical activity was monitored in 7 chronically instrumented fetal sheep before and during both saline and cocaine HCl infusions directly to the fetus. Saline infusion to the fetus had no effect on the percentage of time spent in rapid eye movement sleep compared to no infusion (37.5 ± 11.6% vs 46.3 ± 4.6%, mean ± SD, P > 0.1). Cocaine infusion directly to the fetus had no effect on fetal arterial pO 2, but did increase mean arterial pressure from 53.6 ± 15 mmHg to 61.0 ± 21 mmHg ( P < 0.01). In addition, during cocaine infusion, the percentage of time spent in rapid eye movement sleep dropped to 3.9 ± 5.1% ( P < 0.0001) and the average duration of rapid eye movement epochs decreased from 10.1 ± 3.0 min precocaine infusion to 1.9 ± 2.6 min during cocaine infusion ( P < 0.02). The influence of cocaine was noted in a frequency analysis of the electrocorticogram. The amplitude of the energy centered at 1 Hz during cocaine infusion (73.8 ± 4.0 dB) was greater than the amplitude during rapid eye movement sleep (65.5 ± 4.7 dB) and less than the amplitude during non-rapid eye movement periods (79.9 ± 4.5 dB) ( P = 0.01). Cocaine appears to alter fetal behavioral state directly and this may play a role in the abnormal behavior in newborn infants exposed to cocaine in utero.

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