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Despite mounting evidence of detrimental effects of maternal smoking on fetuses, including still birth, intrauterine growth restriction (IUGR), and sudden infant death syndrome (SIDS) among many others, the prevalence of smoking women exceeds 10% in a majority of developed countries (Dessì et al., 2018). For example, in the USA, the prevalence is about 14%(Dessì et al., 2018), and in Poland, this rate is 15–20%(Chełchowska et al., 2018). Pregnancy smoking rates can be much higher in certain sub-populations of these countries, such as for instance, among the indigenous NZ Maori population at rates of 34%—well above the national level of 10%(Humphrey et al., 2016). Smoking cessation is challenging due to multiple reasons, including nicotine addiction, cultural and social-economic status, and resistance to life-style change (Dessì et al., 2018). Early interventions are required to reverse the pathological course exposing the fetus to hazards from smoking. This demands a precise understanding of the underlying etiologies and evaluating appropriate pharmaceutical targets. We are particularly interested in pathologies emerging in the fetal cardiovascular system (CVS) due to smoking exposure (Dikalov et al., 2019). Indeed, active and passive maternal smoking cause hemodynamic changes in major fetal blood vessels such as the umbilical arteries (UAs)—a biomarker for impaired feto-placental circulation (Westergaard et al., 2001).

Unfortunately, examining the molecular and hemodynamic mechanisms of fetuses in utero is difficult due to ethical and technical reasons. Instead, ex vivo and in vitro experiments are performed; eg …