Читать книгу Protocols for High-Risk Pregnancies - Группа авторов - Страница 22

There are several mechanisms which have been identified and proposed to explain adverse obstetrical and fetal outcomes associated with maternal nicotine exposure through cigarette smoking, e‐cigarette use or other smokeless routes. Nicotine crosses the placenta and can be detected in the fetal circulation at levels that exceed maternal concentrations by 15%, while amniotic fluid concentrations of nicotine are 88% higher than maternal plasma. Nicotine has been identified to impair uterine vascular function during pregnancy, by increasing vascular resistance and decreasing uterine artery blood flow. Carbon monoxide is also released during smoking and can be detected in the fetal circulation at levels that are 15% higher than maternal levels. It has a higher affinity for hemoglobin than oxygen to form the compound carboxyhemoglobin that shifts the oxygen dissociation curve to the left. Consequently, the availability of oxygen to fetal tissues is decreased. Beyond nicotine and carbon monoxide, tobacco smoke contains thousands of compounds that may have adverse effects on the developing fetus. For example, levels of cyanide in the circulation are higher in smokers, a substance that is toxic to rapidly dividing cells. In addition, nicotine can affect long‐term function through epigenetic changes

Nicotine replacement therapies such as gum, lozenges, patches or inhalers provide a sustained, yet lower level of nicotine compared to cigarettes. Similar effects of stillbirth, preterm birth, and low birthweight have been documented with use of these therapies, which can be attributed to impaired uterine vascular function due to the nicotine exposure. Vaping or e‐cigarette aerosol may also expose the user to volatile organic compounds and heavy metals, in addition to the nicotine or other substances commonly delivered. More research is needed regarding the effects of e‐cigarette on the developing fetus.