Sudden infant death syndrome: a preconditioning approach to acute arterial hypoxemia.
The blood hemoglobin F (HbF) concentration increases in response to chronic arterial hypoxemia and is abnormally elevated in sudden infant death syndrome (SIDS) post-mortem indicating a need for greater oxygen affinity of hemoglobin (Hb) or diminished oxygen usage by tissues or both. Modifying Hb oxygen affinity in rats revealed that increased, rather than decreased, hemoglobin-oxygen affinity permitted survival at greatly reduced environmental oxygen pressures equivalent to high altitude. Decreased Hb-oxygen affinity resulted in bradycardia 5-10 minutes before death. Cardiorespiratory recordings from infants dying suddenly and unexpectedly at home demonstrated cardiovascular failure with hypotension and bradycardia, rather than a cessation of breathing.A fall in blood pressure and acidosis due to hypoxemia in combination with reduced arterial oxygen saturation leads to circulatory failure, heart failure and death. It is speculated that the final mechanism of SIDS mimics failure to survive at high altitudes and very low environmental oxygen pressures when low arterial oxygen pressures combine with decreased Hb-oxygen affinity lead to severe hypoxemia and death.
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D000818:Animals; D001158:Arteries; D005319:Fetal Hemoglobin / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D007223:Infant; D010100:Oxygen / Q000097:blood; D051381:Rats; D013398:Sudden Infant Death / Q000097:blood*
D005319:Fetal Hemoglobin; D010100:Oxygen