Elevated body temperature enhances the laryngeal chemoreflex in decerebrate piglets.

Hyperthermia and reflex apnea may both contribute to sudden infant death syndrome (SIDS). Therefore, we investigated the effect of increased body temperature on the inhibition of breathing produced by water injected into the larynx, which elicits the laryngeal chemoreflex (LCR). We studied decerebrated, vagotomized, neonatal piglets aged 3-15 days. Blood pressure, end-tidal CO(2), body temperature, and phrenic nerve activity were recorded. To elicit the LCR, we infused 0.1 ml of distilled water through a polyethylene tube passed through the nose and positioned just rostral to the larynx. Three to five LCR trials were performed with the piglet at normal body temperature. The animal's core body temperature was raised by approximately 2.5 degrees C, and three to five LCR trials were performed before the animal was cooled, and three to five LCR trials were repeated. The respiratory inhibition associated with the LCR was substantially prolonged when body temperature was elevated. Thus elevated body temperature may contribute to the pathogenesis of SIDS by increasing the inhibitory effects of the LCR.

[1]  K. O'Halloran,et al.  Ventilatory and upper-airway resistance responses to upper-airway cooling and CO2 in anaesthetised rats , 1994, Pflügers Archiv.

[2]  G. J. Mellenbergh,et al.  Risk and preventive factors for cot death in The Netherlands, a low-incidence country , 1998, European Journal of Pediatrics.

[3]  F. Marchal,et al.  Reflex Apnea from Laryngeal Chemo-Stimulation in the Sleeping Premature Newborn Lamb , 1982, Pediatric Research.

[4]  R. Gilbert,et al.  Interaction between bedding and sleeping position in the sudden infant death syndrome: a population based case-control study. , 1990, BMJ.

[5]  D. Bartlett,et al.  Responses of laryngeal receptors to intralaryngeal CO2 in the cat. , 1992, The Journal of physiology.

[6]  P. Richardson,et al.  The reflex effects of intralaryngeal carbon dioxide on the pattern of breathing , 1973, The Journal of physiology.

[7]  C. Sasaki,et al.  Effect of Hyperthermia on the Laryngeal Closure Reflex , 1983, The Annals of otology, rhinology, and laryngology.

[8]  H. Jeffery,et al.  Why the Prone Position Is a Risk Factor for Sudden Infant Death Syndrome , 1999, Pediatrics.

[9]  John Kattwinkel,et al.  Changing Concepts of Sudden Infant Death Syndrome: Implications for Infant Sleeping Environment and Sleep Position , 2000, Pediatrics.

[10]  J Golding,et al.  Environment of infants during sleep and risk of the sudden infant death syndrome: results of 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy , 1996, BMJ.

[11]  Task Force on Infant Sleep Position.  Changing concepts of SIDS : Implications for infant sleeping environment and sleep position , 2000 .

[12]  W. Guntheroth,et al.  Thermal Stress in Sudden Infant Death: Is There an Ambiguity With the Rebreathing Hypothesis? , 2001, Pediatrics.

[13]  M. Schootman,et al.  Heat stress and sudden infant death syndrome incidence: a United States population epidemiologic study. , 2004, Pediatrics.

[14]  B. Thach,et al.  Unintentional suffocation by rebreathing: a death scene and physiologic investigation of a possible cause of sudden infant death. , 1993, The Journal of pediatrics.

[15]  N. Simionescu,et al.  The Cardiovascular System , 1983 .

[16]  B. Thach,et al.  Sudden infant death syndrome: can gastroesophageal reflux cause sudden infant death? , 2000, The American journal of medicine.

[17]  B. Taylor,et al.  SLEEPING POSITION AND INFANT BEDDING MAY PREDISPOSE TO HYPERTHERMIA AND THE SUDDEN INFANT DEATH SYNDROME , 1989, The Lancet.

[18]  P. Fleming,et al.  Sudden unexplained infant death in 20 regions in Europe: case control study , 2004, The Lancet.

[19]  J. Daling,et al.  Risk Factors for Sudden Infant Death Syndrome: Changes Associated With Sleep Position Recommendations , 2002 .

[20]  G. J. Mellenbergh,et al.  Case-control study of current validity of previously described risk factors for SIDS in the Netherlands , 1998, Archives of disease in childhood.

[21]  H. Kinney,et al.  Decreased Kainate Receptor Binding in the Arcuate Nucleus of the Sudden Infant Death Syndrome , 1997, Journal of neuropathology and experimental neurology.

[22]  A. Bradford,et al.  Effect of upper airway cooling and CO2 on diaphragm and geniohyoid muscle activity in the rat. , 1996, The European respiratory journal.

[23]  J. Leiter,et al.  Alteration of ventilatory activity by intralaryngeal CO2 in the cat. , 1992, The Journal of physiology.

[24]  B. Thach,et al.  Inhibitory effects of hyperthermia on mechanisms involved in autoresuscitation from hypoxic apnea in mice: a model for thermal stress causing SIDS. , 2004, Journal of applied physiology.

[25]  H. Kinney,et al.  Decreased Serotonergic Receptor Binding in Rhombic Lip‐Derived Regions of the Medulla Oblongata in the Sudden Infant Death Syndrome , 2000, Journal of neuropathology and experimental neurology.

[26]  H. Kinney,et al.  Decreased muscarinic receptor binding in the arcuate nucleus in sudden infant death syndrome , 1995, Science.

[27]  S. Downing,et al.  Laryngeal chemosensitivity: a possible mechanism for sudden infant death. , 1975, Pediatrics.

[28]  J. Leiter,et al.  Prolongation of the laryngeal chemoreflex after inhibition of the rostral ventral medulla in piglets: a role in SIDS? , 2003, Journal of applied physiology.

[29]  A. Wilkinson,et al.  Proceedings: Cardiovascular changes in new-born lambs during apnoea induced by stimulation of laryngeal receptors with water. , 1976, The Journal of physiology.

[30]  B. Graham,et al.  Respiratory Syncytial Virus Infection Reinforces Reflex Apnea in Young Lambs , 1992, Pediatric Research.

[31]  A. Stanton.  OVERHEATING AND COT DEATH , 1984, The Lancet.

[32]  B. Taylor,et al.  Sleep position, autonomic function, and arousal , 1998, Archives of disease in childhood. Fetal and neonatal edition.

[33]  T. Dwyer,et al.  Factors potentiating the risk of sudden infant death syndrome associated with the prone position. , 1993, The New England journal of medicine.

[34]  H. Kinney,et al.  A perspective on neuropathologic findings in victims of the sudden infant death syndrome: the triple-risk model. , 1994, Biology of the neonate.

[35]  J. T. Shepherd,et al.  Peripheral circulation and organ blood flow , 1983 .

[36]  M. Wailoo,et al.  Prone sleeping infants have a reduced ability to lose heat. , 1995, Early human development.

[37]  T. Rothämel,et al.  Body and head position, covering of the head by bedding and risk of sudden infant death (SID) , 1998, International Journal of Legal Medicine.

[38]  M. Malloy.  Trends in postneonatal aspiration deaths and reclassification of sudden infant death syndrome: impact of the "Back to Sleep" program. , 2002, Pediatrics.

[39]  Daniel M. Peraza,et al.  Enhanced baroreflex-mediated inhibition of respiration after muscimol dialysis in the rostroventral medulla. , 2002, Journal of applied physiology.

[40]  D. Bartlett,et al.  Chemical specificity of a laryngeal apneic reflex in puppies. , 1982, Journal of applied physiology: respiratory, environmental and exercise physiology.

[41]  E. Nattie,et al.  Muscimol dialysis in the rostral ventral medulla reduced the CO(2) response in awake and sleeping piglets. , 2001, Journal of applied physiology.