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Prenatal nicotine exposure can lead to cardiac function reprogramming in adult offspring
May 01, 2007Female offspring more likely to be impacted than males, lab study finds
WASHINGTON -- At least 11 percent of American women smoke during pregnancy. The negative effects of nicotine exposure to their fetuses and newborns are significant. A 2004 report by the Surgeon General, for example, found that women who smoked during pregnancy had children who were at a three times higher risk for SIDS than were the offspring of non-smokers. Now, a new study using laboratory rats, provides strong evidence that the effects of maternal smoking during the prenatal period of life can lead to cardiac vascular dysfunction beyond the formative years -- and into adulthood.
The finding is part of a new study entitled Effect of Prenatal Nicotine Exposure on Coronary Flow in Adult Offspring: A Gender Dichotomy. It was conducted by Daliao Xiao, Jennifer Lawrence, Shumei Yang, and Lubo Zhang, all of the Center for Perinatal Biology, Loma Linda University, School of Medicine, Loma Linda, and the Department of Chemistry and Biochemistry, California State University, San Bernardino, CA Dr. Zhang will lead a discussion of the findings at the 120th annual meeting of the American Physiological Society (APS; www.the-APS.org), being held as part of the Experimental Biology (EB ¡¦07) meeting. More than 12,000 scientists and researchers are attending the conference, being held April 28-May 2, 2007 at the Washington, DC Convention Center.
Summary of Methodology
Nicotine (2.1 mg/d) was administered via osmotic minipumps placed under the skin throughout gestation and up to ten days after delivery. Hearts were isolated from three month old male and female offspring, and subjected to 25-minutes of mechanical obstruction of blood flow ischemia followed by 60-minutes of myocardial impairment caused by opening of the blockage. Pulmonary artery discharge was collected as an index of coronary flow (ml/min/g heart wet weight).
Summary of Results
The researchers found:
* that nicotine significantly decreased coronary flow in female (10.4¡"0.8 vs. 7.1¡"0.7, P< 0.05) but not in male (9.1¡" 0.5 vs. 9.0¡"0.7, P>0.05) hearts at baseline;
* nicotine treatment significantly decreased coronary flow during reperfusion up to 60-minutes in female, but not in male, hearts.
* prenatal nicotine exposure significantly increased ischemia and reperfusion-induced infarct size in left ventricles and significantly affected post-ischemic recovery of left ventricular function in both male and female offspring. However, the effect of nicotine was significantly more pronounced in females than in males.
Conclusions
The results suggest that prenatal nicotine exposure selectively decreases coronary flow in adult female offspring. The findings suggest that prenatal nicotine exposure causes a reprogramming of cardiac function resulting in an increase in heart susceptibility to ischemia and reperfusion injury in adult offspring. In addition, the effect of nicotine shows a gender dichotomy with females being more susceptible than males.
The selective effect of nicotine on coronary flow in the female heart may contribute to the increased susceptibility of female vs. male hearts, in response to ischemia and reperfusion-induced cardiac damage in animals exposed to prenatal nicotine treatment. Additional study is thus required.
American Physiological Society
Summary of Methodology
Nicotine (2.1 mg/d) was administered via osmotic minipumps placed under the skin throughout gestation and up to ten days after delivery. Hearts were isolated from three month old male and female offspring, and subjected to 25-minutes of mechanical obstruction of blood flow ischemia followed by 60-minutes of myocardial impairment caused by opening of the blockage. Pulmonary artery discharge was collected as an index of coronary flow (ml/min/g heart wet weight).
Summary of Results
The researchers found:
* that nicotine significantly decreased coronary flow in female (10.4¡"0.8 vs. 7.1¡"0.7, P< 0.05) but not in male (9.1¡" 0.5 vs. 9.0¡"0.7, P>0.05) hearts at baseline;
* nicotine treatment significantly decreased coronary flow during reperfusion up to 60-minutes in female, but not in male, hearts.
* prenatal nicotine exposure significantly increased ischemia and reperfusion-induced infarct size in left ventricles and significantly affected post-ischemic recovery of left ventricular function in both male and female offspring. However, the effect of nicotine was significantly more pronounced in females than in males.
Conclusions
The results suggest that prenatal nicotine exposure selectively decreases coronary flow in adult female offspring. The findings suggest that prenatal nicotine exposure causes a reprogramming of cardiac function resulting in an increase in heart susceptibility to ischemia and reperfusion injury in adult offspring. In addition, the effect of nicotine shows a gender dichotomy with females being more susceptible than males.
The selective effect of nicotine on coronary flow in the female heart may contribute to the increased susceptibility of female vs. male hearts, in response to ischemia and reperfusion-induced cardiac damage in animals exposed to prenatal nicotine treatment. Additional study is thus required.
American Physiological Society
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