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Simple drug treatment may prevent nicotine-induced SIDS: Study
June 03, 2009A new study has identified a specific class of pharmaceutical drugs that could be effective in treating babies vulnerable to Sudden Infant Death Syndrome (SIDS), because their mothers smoked during pregnancy.
According to researchers at McMaster University, exposure of the fetus to nicotine results in the inability to respond to decreases in oxygen-known as hypoxia-which may result in a higher incidence of SIDS. In the same study on rats, they found that the diabetic medication 'glibenclamide' can reverse the effects of nicotine exposure, increasing the newborn's ability to respond to hypoxia and likely reducing the incidence of SIDS.
The findings are published today in the Journal of Neuroscience.
"During birth the baby rapidly changes its physiology and anatomy so that it can breathe on its own," explains Josef Buttigieg, lead author who conducted his research as a PhD graduate student in the department of Biology. "The stress of being born induces the release of the hormones adrenaline and noradrenaline-collectively called catecholamines-from the adrenal glands. During birth, these hormones in turn signal the baby's lungs to become ready for air breathing."
For some months after birth, the adrenal glands act as a critical oxygen sensor. A drop in blood oxygen levels will stimulate the release of catecholamines, which in turn signals the baby to take a deep breath, when an infant rolls on its face or has an irregular breathing pattern during sleep, for example. However, the ability to release those hormones during moments of apnea or asphyxia is impaired due to nicotine exposure.
During those episodes, specific proteins sensitive to hypoxia stimulate the cell to release catecholamines. A secondary class of proteins then acts as a 'brake', ensuring the cells do not over excite themselves during this stressful time. However, exposure of the fetus to nicotine results in higher levels of this brake protein.
"The result is like trying to drive your car with the parking brake on. You might go a little bit, but the brakes hold you back," explains Buttigieg. "In this case, the adrenal glands do not release catecholamines during hypoxia -for example during birth or a self-asphyxiation episode-often resulting in death."
But when researchers administered the drug glibenclamide in laboratory rats, which override the brake protein, the adrenal glands were able to respond to oxygen deprivation, therefore reversing the lethality of hypoxia.
"Our initial goal was really to understand how the nervous system regulates oxygen sensitivity of cells in the adrenal gland at a basic research level," says Colin Nurse, academic advisor on the study and a professor in the department of Biology. "We speculated that chemicals released from nerves might interact with adrenal cells and cause them to lose oxygen sensitivity. It turns out that nicotine mimics the effects of one of these chemicals, thereby allowing us to test the idea. The present study was significant in that it led to a mechanistic understanding of how nicotine works in this context."
McMaster University
"During birth the baby rapidly changes its physiology and anatomy so that it can breathe on its own," explains Josef Buttigieg, lead author who conducted his research as a PhD graduate student in the department of Biology. "The stress of being born induces the release of the hormones adrenaline and noradrenaline-collectively called catecholamines-from the adrenal glands. During birth, these hormones in turn signal the baby's lungs to become ready for air breathing."
For some months after birth, the adrenal glands act as a critical oxygen sensor. A drop in blood oxygen levels will stimulate the release of catecholamines, which in turn signals the baby to take a deep breath, when an infant rolls on its face or has an irregular breathing pattern during sleep, for example. However, the ability to release those hormones during moments of apnea or asphyxia is impaired due to nicotine exposure.
During those episodes, specific proteins sensitive to hypoxia stimulate the cell to release catecholamines. A secondary class of proteins then acts as a 'brake', ensuring the cells do not over excite themselves during this stressful time. However, exposure of the fetus to nicotine results in higher levels of this brake protein.
"The result is like trying to drive your car with the parking brake on. You might go a little bit, but the brakes hold you back," explains Buttigieg. "In this case, the adrenal glands do not release catecholamines during hypoxia -for example during birth or a self-asphyxiation episode-often resulting in death."
But when researchers administered the drug glibenclamide in laboratory rats, which override the brake protein, the adrenal glands were able to respond to oxygen deprivation, therefore reversing the lethality of hypoxia.
"Our initial goal was really to understand how the nervous system regulates oxygen sensitivity of cells in the adrenal gland at a basic research level," says Colin Nurse, academic advisor on the study and a professor in the department of Biology. "We speculated that chemicals released from nerves might interact with adrenal cells and cause them to lose oxygen sensitivity. It turns out that nicotine mimics the effects of one of these chemicals, thereby allowing us to test the idea. The present study was significant in that it led to a mechanistic understanding of how nicotine works in this context."
McMaster University
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Maternal smoking may alter the arousal process of infants, increasing their risk for SIDS
A study in the April 1 issue of the journal SLEEP shows that maternal smoking is associated with an impaired infant arousal process that may increase the risk for sudden infant death syndrome (SIDS). The authors suggest that maternal smoking has replaced stomach sleeping as the greatest modifiable risk factor for SIDS.
New study identifies risk factors in severity of 'flat head syndrome' in babies
A new study by physician researchers from Hasbro Children's Hospital and Children's Hospital Boston identifies risk factors for the severity of asymmetrical head shapes, known as deformational plagiocephaly (DP), or more commonly as flat head syndrome. The study was published in the March 2009 edition of the Journal of Craniofacial Surgery.
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