Sudden infant death syndrome: near-weightlessness and delayed neural transformation.
Dilation of the pulmonary arteries and increased pulmonary blood volume are recorded in sudden infant death syndrome and in infants living at low barometric pressures (high altitude). Low barometric pressure leads to chronic alveolar hypoxia (1,2). There is diversion and loss of body-fluid under conditions of microgravity (near-weightlessness) encountered in human space-travel and prolonged bedrest (3). The condition mimics shock and oligemia (4,5). The human neonate has underdeveloped postural mechanisms and low muscle-power. A transformation begins at about two months of age, which enables the human infant to adapt to the extrauterine environment (6). The neonate resembles the space traveller who, in a near-weightlessness antigravity environment, develops baroreceptor incompetence, visceral and venous congestion and oliguria. The low birthweight infant displays many of the disorders of the space traveller, viz. poor circulation, high blood-glucose, insulin resistance, weak muscles, slow gut absorption and bone demineralization (7-10). These conditions are virtually identical with the internal adjustments the body makes on lying down (negative gravity or near-weightlessness). We discuss the similarities of sudden infant death syndrome to low barometric pressure environment, orthostatic intolerance, the Pickwickian syndrome and X disease.
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D000532:Altitude Sickness / Q000503:physiopathology; D000818:Animals; D001933:Brain Stem / Q000503:physiopathology; D005260:Female; D006801:Humans; D007223:Infant; D008954:Models, Biological; D010845:Obesity Hypoventilation Syndrome / Q000503:physiopathology; D011247:Pregnancy; D011652:Pulmonary Circulation; D013398:Sudden Infant Death / Q000209:etiology*; D014893:Weightlessness / Q000009:adverse effects