Not exact matches
In animal models,
exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In
human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal
exposure to tobacco
smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of
smoking mothers exhibit impaired arousal patterns
to trigeminal stimulation in proportion
to urinary cotinine levels.35 It is important
to note also that prenatal
exposure to tobacco
smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response
to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability
to SIDS.
Chronic
cigarette smoke exposure, as noted in many
human cancers, tends
to block these cell maturation genes from properly turning on, says Baylin.
The amount of nicotine in the rats» blood after
exposure to cigarette smoke was similar
to the amount in blood after
humans have
smoked one
cigarette, confirming that the
exposure conditions were relevant
to the real world.
This is the first study
to examine the effects of prenatal
exposure to methamphetamine, marijuana, and
cigarette smoking on
human placental development.
Three recent experimental studies focused on low consumption /
exposure.949596 In one study, 29 smokers each consumed a single
cigarette, immediately after which they had a significant decrease in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study,
human coronary artery endothelial cells were exposed
to the
smoke equivalent
to one
cigarette, which led
to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered
to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed
to the vapour from one e -
cigarette.95 A study exposed adult mice
to low intensity tobacco
smoke (two
cigarettes) for one
to two months and found adverse histopathological effects on brain cells.96