Peripheral Chemoreceptors and Sudden Infant Death Syndrome: A Wide Open Problem

This review will focus on the basic mechanisms of the peripheral chemoreceptors elicited by studies on mature chemoreceptors and on the alterations observed in these structures related to sudden infant death. The integrated response of the peripheral chemoreceptors consists of the transduction of alterations in the chemical milieu, regulating the temperature of their environment to alterations in cardiovascular and respiratory performance. Over the years, much has been written about the relative importance of the carotid and aortic bodies in the peripheral chemoreceptor response, and it is therefore worthwhile to consider the current state-of-the-art on that issue. Several lines of evidence have suggested that abnormalities in chemoreception may play a role in central hypoventilation syndromes. The sudden infant death syndrome (SIDS) involves a failure of respiration and affects infants in their early postnatal months. Unstable respiratory activity during sleep, prolonged sleep apnea, and oropharyngeal/laryngeal dysfunction induced by liquid stimulation of the upper airways have been postulated to be implicated in its genesis. It has also been found that in comparison with normal infants, infants suffering from the “aborted syndrome” (near-miss infants) are hypoventilated during quiet sleep, and have an impaired ventilatory response to carbon dioxide breathing.