Effects of apomorphine and haloperidol in fetal lambs.

Injections of 100 micrograms apomorphine (I.A.) in intact unanaesthetized fetal lambs resulted in the onset of low‐voltage electrocortical activity if not already present, onset or an increase in amplitude of fetal breathing movements, and in about 50% of experiments, onset or an increase in skeletal muscle activity. These responses also occurred during isocapnic hypoxia, though the stimulation of breathing was less than in normoxic lambs. Apomorphine had no consistent effects on the blood gases, pH, heart rate or blood pressure. In fetal lambs with the carotid nerves and vago‐sympathetic trunks sectioned, apomorphine had the same effects as in intact lambs, except that there was a small fall in arterial O2 pressure (Pa,O2). Haloperidol (0.5‐1 mg I.V.) had no effect on spontaneous breathing movements or electrocortical activity, but blocked all responses to apomorphine for several hours. Dopamine (up to 4 mg I.V.) caused an increase in arterial pressure accompanied by bradycardia, but had no effect on breathing movements or electrocortical activity. After suprapontine brain‐stem transection, the electrocortical response to apomorphine was reduced. The respiratory response was lost or reversed, with apomorphine causing a reduction in amplitude of breathing. Haloperidol reduced the incidence of breathing movements for several hours in brain‐stem‐transected fetuses. We conclude that there is a central pathway, including at least one dopaminergic synapse and with components above the pons, which can stimulate fetal motor activity and breathing. It does not appear to be tonically active and its normal function is unknown.