A triple-risk model for the sudden infant death syndrome (SIDS) and the apparent life-threatening episode (ALTE): the stressed magnesium deficient weanling rat.
A triple risk model for the sudden infant death syndrome (SIDS) as described by Filiano and Kinney involves the intersection of three risks: (1) a vulnerable infant, (2) a critical developmental period in homeostatic control, and (3) an exogenous stressor(s). The triple risk model aptly describes the dynamics of an animal model for SIDS: (1) a vulnerable animal that is young and magnesium deficient: (2) a critical developmental period revealed by hyperirritability, labile cardiovascular and respiratory control; and (3) an exogenous stressor such as soft, high-pitched noise; motion or handling; or a chill. Together these three risks may trigger a shock-like episode of apnea, unconsciousness and bradycardia. The lung is the shock organ. An animal that dies quietly or after physical activity following the episode, models SIDS. However, if the shock-like episode resolves spontaneously or after resuscitation, the survivor is a model for an apparent life-threatening episode (ALTE). If, while still in the critical developmental period the ALTE survivor is stressed again, there is a risk for a recurrent episode, with the final outcome still unpredictable but with increasing risk for SIDS with multiple recurrences. The purpose of this communication is to present an illustrated review of the magnesium deficient weanling rat as an animal model for SIDS/ALTE, showing pertinent physical, electrocardiographic and pathological features. In the weanling rat, magnesium deficiency appears to be the single common pathway upon which multiple stressors may impinge to produce sudden death during the relatively brief critical developmental period, while magnesium supplements may protect the animal. If significant magnesium deficiency is subsequently diagnosed in a properly controlled study of human SIDS tissue, it is likely that a high proportion of SIDS deaths could be prevented by simple oral magnesium supplementation to infants during the first critical weeks and months of life.
Caddell
J L
JL
Department of Pediatrics, Thomas Jefferson University, Philadelphia, PA 19107-5083, USA.
D000818:Animals; D004032:Diet; D004195:Disease Models, Animal; D004562:Electrocardiography; D006706:Homeostasis; D006801:Humans; D007223:Infant; D008168:Lung / Q000473:pathology* / Q000503:physiopathology; D008275:Magnesium Deficiency / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012128:Respiratory Distress Syndrome / Q000473:pathology / Q000503:physiopathology*; D012307:Risk Factors; D013398:Sudden Infant Death / Q000209:etiology* / Q000473:pathology