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HYPOXIC INHIBITION OF BREATHING AND MOTOR ACTIVITY IN THE FOETUS AND NEWBORN
Author(s) -
Walker David W.
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02062.x
Subject(s) - pons , hypoxia (environmental) , fetus , respiratory system , medicine , neuroscience , inhibitory postsynaptic potential , parabrachial nucleus , brainstem , anatomy , endocrinology , anesthesia , biology , chemistry , pregnancy , genetics , organic chemistry , oxygen
SUMMARY In fetal animals hypoxia of rapid onset causes cessation of breathing movements, electro‐ocular activity and decrease of muscle tone. These effects last several hours and are in contrast to the hypernoea and behavioural activation which occurs during hypoxia soon after birth and in the adult. Transection and lesion studies in fetal sheep suggest that hypoxia activates a descending inhibition of respiratory and other motor activities which either originates in the pons or is conveyed to medullary and spinal levels of the neuraxis by fibres through the pons in the region of the Kolliker‐Fuse nucleus. Recently, using FOS immunohistochemistry we have identified cells in the medial parabrachial complex which are activated by hypoxia in fetal sheep, but not newborn lambs. It is proposed that these cells have descending inhibitory connections with respiratory and spinal motor pathways, but the precise anatomy and neuro‐chemistry of such pathways is unknown. It is not known if the parabrachial cells are directly sensitive to low P o 2 or receive input from other centres or peripheral receptors which monitor arterial P o 2 in the foetus. Nor is it known why these cells are not activated by low P o 2 after birth.