Caddell J L
Department of Pediatrics, Thomas Jefferson University, Philadelphia, PA 19107-5083, USA.
Magnes Res. 2001 Sep;14(3):227-38.
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.
菲利亚诺和金尼所描述的婴儿猝死综合征(SIDS)三重风险模型涉及三种风险的交集:(1)易损婴儿,(2)稳态控制中的关键发育阶段,以及(3)一种或多种外源性应激源。该三重风险模型恰当地描述了SIDS动物模型的动态过程:(1)年幼且缺镁的易损动物;(2)由过度易激惹、不稳定的心血管和呼吸控制所揭示的关键发育阶段;以及(3)外源性应激源,如轻柔、高音调的噪音;运动或处理;或寒冷。这三种风险共同作用可能引发类似休克的呼吸暂停、意识丧失和心动过缓发作。肺是休克器官。在发作后安静死亡或在体力活动后死亡的动物可模拟SIDS。然而,如果类似休克的发作自行缓解或复苏后缓解,幸存者则是明显危及生命事件(ALTE)的模型。如果在关键发育阶段,ALTE幸存者再次受到应激,就有复发发作的风险,最终结果仍然不可预测,但随着多次复发,SIDS的风险会增加。本交流的目的是展示对缺镁断奶大鼠作为SIDS/ALTE动物模型的图文综述,展示相关的身体、心电图和病理特征。在断奶大鼠中,镁缺乏似乎是多种应激源可能在相对短暂的关键发育阶段作用导致猝死的单一共同途径,而补充镁可能保护动物。如果在对人类SIDS组织进行的适当对照研究中随后诊断出严重镁缺乏,那么在婴儿生命的最初关键几周和几个月通过简单口服补充镁,很可能可以预防很大比例的SIDS死亡。