A cardioinhibitory area in the central tegmental field of the midbrain (CIM) was studied in cats under
chloralose-
urethane anesthesia. Electrical and chemical (
glutamate and
DL-homocysteic acid) stimulations in this area produced marked
bradycardia accompanied by mostly
hypotension or minimal change in arterial pressure and by occasional
hypertension particularly in the dorsal portion. CIM excitation potentiated the reflex
bradycardia induced by IV
phenylephrine, while bilateral electrolytic lesion of CIM neither changed the resting cardiovascular parameters nor the reflex
bradycardia. The CIM
bradycardia was not affected by supracollicular decerebration, but substantially reduced by unilateral
vagotomy and completely eliminated by bilateral
vagotomy. Destruction of the ambiguus nucleus (NA) and solitary and dorsal motor nuclei (NTS/DMV) abolished the
bradycardia. Midline bisection at the midbrain-pontine level only slightly reduced the
bradycardia while at the medullary level it was moderately attenuated. Electrolytic lesion of the cardioinhibitory area in gigantocellular reticular nucleus (GRN) abolished the
bradycardia. These findings suggest that CIM is an independent mechanism which may send axons to GRN from which the axons may in turn synapse with the NTS/DMV complex and NA. Its final output may utilize both vagus nerves to modulate baroreceptor reflex in promoting
bradycardia.