One of the most common reasons of congenital birth defects is prenatal substance abuse. The severity of the defect depends on the amount of substance abused and the period of gestation during which substance is abused. Although prenatal substance abuse is common during the first trimester, some women continue the abuse well into their second trimester, which is considered the peak period for fetal neurogenesis and angiogenesis. Thus, evaluating the changes in fetal brain vasculature caused by maternal exposure to different teratogens at the second trimester equivalent period is crucial. In this study we use correlation mapping optical coherence angiography (cm-OCA), a functional extension of optical coherence tomography, to image changes in murine fetal brain vasculature caused due to prenatal exposure to ethanol, cannabinoids, or nicotine. Results showed significant vasoconstriction in all three cases.
In the United States, 20% of pregnant women are estimated to smoke, thus affecting 800,000 babies annually. Maternal nicotine exposure is known to have several detrimental effects on the developing fetus including intrauterine growth restriction, perinatal mortality and morbidity, placental abruption, and other childhood disorders. In humans, studies evaluating the association between maternal cigarette smoking during pregnancy and behavioral development in offsprings have shown negative influences of nicotine on brain development. Although several studies have documented lower birth weights, morphological and behavioral changes, not much has been done evaluating the acute changes in brain vasculature after prenatal exposure to nicotine. This work uses correlation mapping optical coherence angiography (cm-OCA), a functional extension of optical coherence tomography, to evaluate changes in murine fetal brain vasculature, in utero, minutes after maternal nicotine exposure. A rapid and significant decrease in vasculature was observed compared to the sham group.
Prenatal substance abuse is one of the main causes of birth defects. Depending upon the substance being abused and the period of gestation during which the abuse happens, the severity of the defect is determined. Although prenatal substance abuse during the first trimester is common, the prevalence of unplanned pregnancies in the United States have led to women continuing their substance abuse well into the second trimester. The second trimester is the peak period for fetal neurogenesis and angiogenesis. Hence, any exposure to teratogens during this period is known to hinder brain development. Several studies have documented changes in morphology and behavior due to exposure to teratogens during this period. However, not a lot is known about the changes in vasculature in the developing brain. In this study, we used angiographic optical coherence tomography, a functional extension of optical coherence tomography, to image acute vasculature changes in the fetal brain caused due to prenatal exposure to ethanol, nicotine, and synthetic cannabinoids (SCB). Results showed a significant decrease in vasculature in all three cases compared to their respective sham groups.
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