Prenatal cocaine exposure influences the growth and life span of laboratory rats.

Laboratory rats prenatally exposed to alcohol, nicotine, amphetamine, undernutrition or hypoxia can exhibit shortened life span and other signs of enhanced age-related degeneration. We evaluated the possibility of similar effects following prenatal cocaine exposure. Pregnant rats received 20 or 40 mg/kg cocaine HCl subcutaneously (C20, C40), twice daily, from gestation days (GD) 7-20. Untreated control (UTC) and pair-fed control (PFC) groups were also used. The pregnant C40, C20, and PFC dams ate less food and gained less weight than the UTC dams did. The pregnant C40 and C20 dams drank more water than the UTC dams did, and the pregnant PFC dams drank less than the UTC dams did. The C40 and PFC offspring had delayed earflap openings. The C40 male and female offspring had lower birth weights than their cohorts in the other three groups. The C40 female and male offspring remained significantly underweight until postnatal day (PND) 28 and PND56, respectively. During young adulthood, the males and females in the C20, C40, and PFC groups had normal body weights. During old adulthood, however, the C20 and C40 males and the C20, C40, and PFC females developed reduced body weights as compared with their UTC cohorts. The C20 and C40 male offspring and the C20, C40, and PFC female offspring also had life spans that were 7-12% shorter than that of their UTC cohorts. Thus, groups that showed reduced body weights in old age also showed shorter life spans. These results provided converging evidence that prenatal cocaine exposure caused enhanced age-related degeneration. Observations on cardiac and other organ pathology were also made. Health implications for children born to cocaine-abusing women are discussed.