Our previous study showed that prenatal
nicotine exposure could increase the heart rate of adult male offspring rats, but little is known about the mechanism. The aim of this study was to investigate the mechanism.
Nicotine was subcutaneously administered to pregnant rats at a dose of 1.5mgkg(-1) from the gestational days 3-21; the control group received the same volume of saline by the same route. The offsprings' heart weight, ejection function, ultrastructure, and blood
hormones were determined. The present study exhibited that prenatal
nicotine exposure significantly decreased the offsprings' heart and
body weight at gestational day 21 and at day 15 after birth, but had no effect on the heart and
body weight at 90 days after birth. The hearts were fibrosed in the
nicotine exposed male offsprings, and the heart ejection functions of the
nicotine male offsprings at 90 days after birth were decreased, including SV, FS and EF. In addition, prenatal
nicotine exposure significantly increased the offspring's blood
adrenaline and
norepinephrine levels. These data suggest that the increased heart rate caused by prenatal
nicotine exposure may be a result of myocardial
fibrosis, which leads to heart function decreases, and these data imply a myocardial
fibrosis risk of prenatal
nicotine exposure.