Sudden infant death syndrome and the modulation of neuropeptides released during shock.
It is generally accepted that sudden infant death syndrome (SIDS) victims fail to survive relatively minor stress in infancy. My hypothesis is that failure to orchestrate the endocrine response in stress leads to excessive release of neutral-endopeptidase-sensitive peptide substrates that enhance lethality. The 'quick zinc' response Reid recorded in livestock with circulatory shock is described. It is concluded that the failure to mount an endocrine response leads to SIDS.
Reid
G M
GM
D000818:Animals; D005260:Female; D005315:Fetal Diseases / Q000503:physiopathology; D006801:Humans; D007223:Infant; D008954:Models, Biological; D009479:Neuropeptides / Q000502:physiology*; D011247:Pregnancy; D012769:Shock / Q000503:physiopathology*; D013312:Stress, Physiological; D013398:Sudden Infant Death / Q000209:etiology*; D015032:Zinc / Q000502:physiology
D009479:Neuropeptides; D015032:Zinc