Characterization of an esophagocardiovascular reflex in the rat.

A cardiovascular reflex evoked by esophageal distension (ECR) in urethan-anesthetized male Sprague-Dawley rats was studied to 1) determine whether the relevant sensory input from the esophagus is conveyed by vagal and/or spinal afferents and 2) evaluate the effects and sites of action of antinociceptive agents. Esophageal distension evoked a rise in arterial blood pressure and heart rate that increased linearly with the log of inflation pressure (25-150 mmHg). Distension (100 mmHg for 20 s) of the lower esophagus was a more effective stimulus than distension of the upper esophagus. The ECR was attenuated by unilateral and abolished by bilateral cervical vagotomy and dose dependently inhibited by morphine (1.0-4.0 mg/kg iv) or by intrathecal (T4-T5) administration of dexmedetomidine (DX, 0.05-0.5 microgram), but not by intrathecal (T4-T5) morphine (4-16 micrograms) or intrathecal (L1-L2) or intravenous DX (0.05-0.5 microgram). The ECR was also inhibited by capsaicin and by the topical administration of DX or morphine to the solitary complex. The pressor response persisted after intravenous pancuronium, scopolamine, and methscopolamine. The ECR circuit appears to consist of vagal afferents, efferent sympathetic preganglionic pathways originating in the thoracic spinal cord, and bulbospinal neurons yet to be identified. This reflex fulfills some criteria of a nociceptive event, but this interpretation requires further investigation.