Abstract 1331 Poster Session IV, Tuesday, 5/4 (poster 273)

Maternal cocaine use during pregnancy has been shown to produce fetal organ system vascular disruption resulting in condition such as neonatal CNS infarction and increased incidence of NEC.

We hypothesized that intrauterine cocaine exposure can decrease regional blood flow velocity in the newborn. Doppler middle cerebral artery (MCA), superior mesenteric artery (SMA) blood flow velocity (BFV), and cardiac output (C.O.) were examined in 7 newborn infants (G.A. 37.25±0.89, B.W. 2.46±0.28) whose urine screens were positive for cocaine metabolites, and 7 non-exposed healthy infants between ages 4 and 48 hrs. before and after a milk feeding.

Results: data in Mean ± SD (Table) There was no difference in MCA mean BFV (Vmean) and cardiac output before and after feeding between control and cocaine exposed infants or within the groups. Likewise, prefeed SMA Vmean BFV of cocaine infants did not differ from control; however, the postprandial increase in mean BFV in cocaine infants demonstrated only a 12.27% (p<0.01) increment in contrast to the 65% (p<0.0002) increment among the non-exposed infants. Thus, effects of antenatal cocaine exposure in the neonates varied between intestinal and cerebral vasculatures. It attenuated the postprandial SMA mean BFV response to feeding without affecting prefeed values, but it did not alter MCA mean BFV or C.O..

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We speculate that prenatal cocaine exposure results in region specific vascular disturbances favoring the cerebral and or vital organ circulation.