Beta-endorphin levels in infant apnea syndrome: a preliminary communication

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Endorphins (β-endorphin and metenkephalin) are naturally occurring, endogenous peptides with opioid properties and potencies more than ten times that of morphine.1, 2 Release of endorphins results in neurotransmitter and neuroendocrine effects in the central nervous system. During stress, endorphins produce analgesia, which can be blocked by naloxone.3 Endorphins can also induce important cardiovascular effects, including hypotension, bradycardia, and peripheral vasodilation.4–6 The respiratory effects of endorphins include bradypnea, apnea, and hypoventilation.7, 8

We have previously reported abnormal serum and cerebrospinal fluid (CSF) β-endorphin levels in children with the obesity-hypoventilation or Pick-wickian syndrome and improvement in ventilatory status with a narcotic antagonist (intravenous naloxone therapy).9, 10 Others have suggested a possible role for endorphins in the sudden infant death syndrome (SIDS)11 and recent reports have implicated enkephalin in transient apnea and respiratory depression in preterm rabbits.12 Narcotic antagonist therapy with naloxone has been used to decrease the duration of primary apnea in neonatal asphyxia.13

The infant apnea syndrome (IAS) is the new name for near-miss SIDS. The IAS characterizes infants between 42 weeks gestational age and 12 months chronological age who experience clinically significant apneas of greater than 10 seconds’ duration, some of whom may require tactile stimulation or rarely even cardiopulmonary resuscitation to abort the apneic episode. Because of controversy as to whether the pathophysiology of the apneas in infants previously identified as near-miss SIDS is the same as in those who die of SIDS, and whether the two entities represent a continuum, we prefer to use IAS rather than . . .



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