scholarly journals 5-HT2A receptor activation is necessary for CO2-induced arousal

2015 ◽  
Vol 114 (1) ◽  
pp. 233-243 ◽  
Author(s):  
Gordon F. Buchanan ◽  
Haleigh R. Smith ◽  
Amanda MacAskill ◽  
George B. Richerson
Keyword(s):  
Sudden Infant Death ◽  
Receptor Activation ◽  
Sudden Infant ◽  
Protective Mechanism ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Wild Type ◽  
Unexpected Death ◽  
Obstructive Sleep ◽  
Embryonic Life

Hypercapnia-induced arousal from sleep is an important protective mechanism pertinent to a number of diseases. Most notably among these are the sudden infant death syndrome, obstructive sleep apnea and sudden unexpected death in epilepsy. Serotonin (5-HT) plays a significant role in hypercapnia-induced arousal. The mechanism of 5-HT's role in this protective response is unknown. Here we sought to identify the specific 5-HT receptor subtype(s) involved in this response. Wild-type mice were pretreated with antagonists against 5-HT receptor subtypes, as well as antagonists against adrenergic, cholinergic, histaminergic, dopaminergic, and orexinergic receptors before challenge with inspired CO2 or hypoxia. Antagonists of 5-HT2A receptors dose-dependently blocked CO2-induced arousal. The 5-HT2C receptor antagonist, RS-102221, and the 5-HT1A receptor agonist, 8-OH-DPAT, attenuated but did not completely block CO2-induced arousal. Blockade of non-5-HT receptors did not affect CO2-induced arousal. None of these drugs had any effect on hypoxia-induced arousal. 5-HT2 receptor agonists were given to mice in which 5-HT neurons had been genetically eliminated during embryonic life ( Lmx1b f/f/p) and which are known to lack CO2-induced arousal. Application of agonists to 5-HT2A, but not 5-HT2C, receptors, dose-dependently restored CO2-induced arousal in these mice. These data identify the 5-HT2A receptor as an important mediator of CO2-induced arousal and suggest that, while 5-HT neurons can be independently activated to drive CO2-induced arousal, in the absence of 5-HT neurons and endogenous 5-HT, 5-HT receptor activation can act in a permissive fashion to facilitate CO2-induced arousal via another as yet unidentified chemosensor system.

Cerebrovascular inflammation after brief episodic hypoxia: modulation by neuronal and endothelial nitric oxide synthase

2004 ◽  
Vol 96 (3) ◽  
pp. 1223-1230 ◽  
Author(s):  
Tamer Altay ◽  
Ernesto R. Gonzales ◽  
T. S. Park ◽  
Jeffrey M. Gidday
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Sudden Infant Death ◽  
No Synthase ◽  
Sudden Infant ◽  
Similar Response ◽  
Wild Type ◽  
Neuroprotective Effects ◽  
Obstructive Sleep ◽  
Episodic Hypoxia

Obstructive sleep apnea, apnea of prematurity, and sudden infant death syndrome are associated with a high risk of morbidity and mortality secondary to the neuronal and cerebrovascular consequences of the associated intermittent hypoxia. We hypothesized that episodic hypoxia (EH) promotes inflammation in the cerebral microcirculation and that nitric oxide (NO) produced by the endothelial and neuronal isoforms of NO synthase (eNOS and nNOS, respectively) modulates this response. Anesthetized and ventilated Swiss-Webster ND4 mice, wild-type mice, and NO synthase knockout mice were subjected to a 1-h period of EH (twelve 30-s periods of hypoxia every 5 min). Four, 24, or 48 h later, mice were reanesthetized for imaging of leukocyte dynamics in the cortical venular microcirculation by epifluorescence videomicroscopy through closed cranial windows. In Swiss-Webster ND4 mice, leukocyte adherence increased 2.1-fold at 4 h, 3.4-fold at 24 h, and 1.8-fold at 48 h relative to time-matched, normoxic controls; there was no evidence of delayed hippocampal CA1 pyramidal cell death. A similar response was noted in wild-type mice. However, in eNOS knockouts, leukocyte-endothelial cell adherence was elevated to 4.4-fold over baseline 24 h after EH, and a significant fraction of these animals showed evidence of delayed CA1 cell death. Conversely, in nNOS knockouts, no increase in adherence was noted at 24 h and CA1 viability remained unaffected. We conclude that NO derived from nNOS promotes an inflammatory response in the cerebrovascular microcirculation after short-term EH and that NO produced by eNOS blunts the extent of this response and exerts neuroprotective effects.

scholarly journals Ten Percent of SIDS Cases are Murder — or are They?

2017 ◽  
Vol 7 (2) ◽  
pp. 163-170 ◽  
Author(s):  
Christopher M. Milroy ◽  
Charis Kepron
Keyword(s):  
Sudden Infant Death ◽  
Current Data ◽  
Related Question ◽  
Sudden Infant ◽  
Court Cases ◽  
Unexpected Death ◽  
Infant Deaths ◽  
Lower Figure ◽  
History Of ◽  
Made In

Sudden infant death syndrome (SIDS) has been used as a cause of death for over four decades. It has allowed deaths of infants to be registered as natural. Within this group of deaths, a certain number have been recognized to be homicides from inflicted smothering rather than being natural or accidental deaths. Research has been conducted using confidential inquires to determine how frequent homicide is in cases called SIDS. This paper traces the history of quoted rates of homicide. Early work suggested the figure was between 2-10% of all SIDS cases, though other workers have suggested figures as high as 20-40%. With the fall in the rate of infant deaths following the “Back to Sleep” campaigns, these figures have been reevaluated. If the higher figures were correct that 20-40% of SIDS were homicides, the fall in infant deaths would be expected to be less than it has been. Current data suggests a much lower figure than 10% of current cases, with much lower overall rates of infant deaths. As well as 10% of SIDS cases having been stated to be homicides, a related question is whether multiple deaths classified as SIDS are really homicides. The paper discusses the maxim that one death is a tragedy, two is suspicious, and three deaths indicate homicide. The paper also looks at court cases and the approach that has been made in prosecutions of sudden unexpected death in infancy as multiple murder.

scholarly journals Aquaporin-1 and aquaporin-9 gene variations in sudden infant death syndrome

2021 ◽  
Author(s):  
Siri Hauge Opdal ◽  
Linda Ferrante ◽  
Torleiv Ole Rognum ◽  
Arne Stray-Pedersen
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Brain Function ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Unexpected Death ◽  
Aquaporin 9 ◽  
Genes Encoding ◽  
External Risk ◽  
The Brain

AbstractSeveral studies have indicated that a vulnerability in the development and regulation of brain function is involved in sudden infant death syndrome (SIDS). The aim of this study was to investigate the genes encoding the brain aquaporins (AQPs) AQP1 and AQP9 in SIDS. The hypothesis was that specific variants of these genes are part of the genetic vulnerability predisposing infants to sudden unexpected death. The study included 168 SIDS cases with a median age of 15.5 (range 2–52) weeks and 372 adolescent/adult deceased controls with a median age of 44 (range 11–91) years. In the AQP1 gene, the rs17159702 CC/CT genotypes were found to be associated with SIDS (p = 0.02). In the AQP9 gene, the combination of a TT genotype of rs8042354, rs2292711 and rs13329178 was more frequent in SIDS cases than in controls (p = 0.03). In the SIDS group, an association was found between genetic variations in the AQP1 gene and maternal smoking and between the 3xTT combination in the AQP9 gene and being found lifeless in a prone position. In conclusion, this study adds further evidence to the involvement of brain aquaporins in SIDS, suggesting that specific variants of AQP genes constitute a genetic predisposition, making the infant vulnerable to sudden death together with external risk factors and probably other genetic factors.

Postmortem genetic analysis of sudden unexpected death in infancy: neonatal genetic screening may enable the prevention of sudden infant death

2017 ◽  
Vol 62 (11) ◽  
pp. 989-995 ◽  
Author(s):  
Yuki Oshima ◽  
Takuma Yamamoto ◽  
Taisuke Ishikawa ◽  
Hiroyuki Mishima ◽  
Aya Matsusue ◽  
...  
Keyword(s):  
Genetic Analysis ◽  
Infant Death ◽  
Genetic Screening ◽  
Sudden Infant Death ◽  
Sudden Unexpected Death ◽  
Sudden Infant ◽  
Unexpected Death

The Uvula and Sudden Infant Death Syndrome

PEDIATRICS ◽  
1984 ◽  
Vol 74 (2) ◽  
pp. 319-320
Author(s):  
CHRISTIAN GUILLEMINAULT
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sleep Apnea Syndrome ◽  
Sudden Infant Death ◽  
Term Infant ◽  
Near Miss ◽  
Sudden Infant ◽  
Obstructive Sleep

In Reply.— Harpey and Renault postulate a relationship between the uvula, obstructive sleep apnea, and sudden infant death syndrome. Although I believe that obstructive sleep apnea syndrome may be one of the mechanisms leading to sudden infant death syndrome, this speculation is extremely controversial. I do concur with Harpey and Renault that obstructive sleep apnea can trigger esophageal reflux. A segment from a sleep recording of a 9-week-old, full-term infant with near-miss sudden infant death syndrome is presented in the Figure.

Mixed and Obstructive Sleep Apnea and Near Miss for Sudden Infant Death Syndrome: 2. Comparison of Near Miss and Normal Control Infants by Age

PEDIATRICS ◽  
1979 ◽  
Vol 64 (6) ◽  
pp. 882-891 ◽  
Author(s):  
Christian Guilleminault ◽  
Ronald Ariagno ◽  
Rowena Korobkin ◽  
Lynn Nagel ◽  
Roger Baldwin ◽  
...  
Keyword(s):  
Normal Control ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Periodic Breathing ◽  
Sudden Infant Death ◽  
Near Miss ◽  
Sudden Infant ◽  
Obstructive Apnea ◽  
Respiratory Events ◽  
Obstructive Sleep

Twenty-nine full-term near miss for sudden infant death syndrome (SIDS) and 30 normal control infants underwent 24-hour polygraphic monitoring. Several types of respiratory events during sleep (eg, central, mixed, and obstructive apnea, periodic breathing) were defined and tabulated. Analysis of these respiratory variables and comparison of groups of near miss and control infants indicated that between 3 weeks and 4½ months of age only one variable was consistently different at a statistically significant level: the number of mixed and obstructive apnea 3 seconds during total sleep time. This study also showed an increase in mixed and obstructive respiratory events during sleep at 6 weeks of age in control as well as in near miss infants.

Sudden Unexpected Death of Two Infants in Baby Carriers

2021 ◽  
Author(s):  
Dennis Storz ◽  
Christof Dame ◽  
Anke Wendt ◽  
Alexander Gratopp ◽  
Christoph Bührer
Keyword(s):  
Risk Factors ◽  
Infant Development ◽  
Sudden Infant Death ◽  
Developed Countries ◽  
Bottle Feeding ◽  
Sudden Unexpected Death ◽  
Sudden Infant ◽  
Unexpected Death ◽  
Sleeping Position ◽  
Prone Sleeping Position

Sudden unexpected death in infancy (SUDI), previously termed sudden infant death syndrome (SIDS), is the second leading cause of death in infants beyond the neonatal period in Germany, and a major cause of infant mortality in economically well developed countries (OECD Health Statistics, 2019). The risk of SUDI peaks at the age of 2–4 months and then decreases continuously till the end of the first year. A complex multifactorial cause, rather than a single characteristic factor, may cause SUDI within a critical period of infant development (Guntheroth WG et al., Pediatrics 2002; 110: e64–e64). Risk factors include prematurity, male gender, bottle-feeding, prone sleeping position, overheating, as well as exposure to smoke amongst others (Carpenter RG et al., Lancet 2004; 363: 185–191). Thus, health professionals consistently advise and educate parents about avoidable risk factors of SUDI at routine well-baby examinations. Since the advent of SUDI prevention strategies in the 1980s, the incidence has decreased 10fold, from 1,55/1.000 live births in 1991 to 0,15/1000 in 2015. This number seems to have reached a steady state (Statistisches Bundesamt Germany, 2015).

scholarly journals Sudden infant death syndrome (SIDS) and the routine otoacoustic emission infant hearing screening test: an epidemiological retrospective case–control study

BMJ Open ◽  
2019 ◽  
Vol 9 (7) ◽  
pp. e030026 ◽  
Author(s):  
Peter S Blair ◽  
Daniel Rubens ◽  
Anna Pease ◽  
Diane Mellers ◽  
Jenny Ingram ◽  
...  
Keyword(s):  
Case Control Study ◽  
Otoacoustic Emission ◽  
Sudden Infant Death ◽  
Case Control ◽  
Sudden Infant ◽  
Unexpected Death ◽  
Retrospective Case ◽  
Bed Sharing ◽  
The Right ◽  
Control Study

ObjectivesTo investigate whether decreased otoacoustic emission (OAE) signal recordings in the right ear are associated with an increased risk of sudden infant death syndrome (SIDS) and to monitor any temporal changes in risk factors.DesignRetrospective case–control study.SettingTelephone interviews with families recruited in England between July 2016 and October 2017 who experienced the unexpected death of a child <4 years old since 2008 and control families recruited from maternity wards in Bristol and Birmingham.ParticipantsWe recruited 91 (89%) of the 102 bereaved families who made initial contact, 64 deaths were under 1 year (sudden unexpected death in infancy) of which 60 remained unexplained (SIDS). Of the 220 control families, 194 (88%) follow-up interviews were conducted. We had analysable hearing data for 24 SIDS infants (40%) and 98 controls (51%).ResultsOAE signals were marginally increased rather than decreased among SIDS infants for the right ear, especially at lower frequencies, but not significantly so. The strongest predictors of SIDS were bed-sharing in hazardous (infant sleeping next to a carer who smoked, drank alcohol or slept on a sofa) circumstances (35% vs 3% controls, p<0.0001), infants found prone (33% vs 3% controls, p<0.0001) and infants whose health in the final week was ‘not good’ (53% vs 9% controls, p<0.0001). The prevalence of maternal smoking during pregnancy among both SIDS mothers (20%) and controls (10%) was much lower than previous studies.ConclusionsHearing data were difficult to obtain; larger numbers would be needed to determine if asymmetrical differences between the right and left ear were a marker for SIDS. A national prospective registry for monitoring and a renewed campaign to a new generation of parents needs to be considered underlining the initial message to place infants on their backs for sleep and the more recent message to avoid bed-sharing in hazardous circumstances.

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