The central control of fetal breathing and skeletal muscle movements.

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Abstract
Breathing movements in the sheep fetus have been observed from a gestational age of about 40 days. From 95 to 115 days fetal breathing movements are almost continuous, interrupted by apnoea rarely exceeding 2 min. From 115 days until term (about 147 days) breathing and movements of the trunk and limbs are episodic. Breathing normally occurs only during rapid-eye-movement sleep as identified by low-voltage cortical electrical activity. Active movements of the neck muscles occur predominantly in high-voltage electrocortical activity. Hypercapnia or acid cerebrospinal fluid perfusion cause an increase in the regularity and depth of breathing when present, and recruit intercostal and laryngeal abductor activity. Isocapnic hypoxia, however, in contrast to the hyperventilation seen postnatally, causes arrest of fetal breathing movements. This effect is due to a central inhibition. Section of the brain stem, from the caudal hypothalamus rostrally, causes dissociation of fetal breathing movements and electrocortical activity into independent rhythms. Section of the brain stem caudally, in the upper pons or at the inferior colliculus, also causes a dissociation of electrocortical activity from breathing movements, which become almost continuous. Isocapnic hypoxia causes an increase in the rate and depth of breathing movements. It is concluded that the arrest of breathing in intact fetal lambs is not due to a direct effect on the respiratory centre in the medulla. The lumbar polysynaptic flexor reflex response becomes episodic after 115 days gestation but, in contrast to fetal breathing movements, is enhanced during high-voltage electrocortical activity. Isocapnic hypoxia arrests movements of the fetal limbs and trunk and inhibits the lumbar flexor reflex. This inhibition of the reflex is prevented by section of the spinal cord at T12, but persists after section of the brain stem in the upper pons. It is attributed to an action on the medulla, independent of the systemic arterial chemoreceptors. Small doses of pentobarbitone (5 mg/kg) cause arrest of fetal breathing movements by a suprapontine mechanism, abolished by brain stem transection, and inhibition of the lumbar flexor reflex by an action on the spinal cord, persisting after transection at T12. Inhibitors of prostaglandin synthetase (indomethacin, meclofenamate or aspirin) induce continuous fetal breathing movements, while prostaglandin E2 arrests fetal breathing. The site of action is on the medulla, as shown by section of the brain stem and of afferents from the systemic arterial chemoreceptors.(ABSTRACT TRUNCATED AT 400 WORDS)