One objective of this study was to examine a mechanism for the inability of patients to distinguish esophageal pain from cardiac pain. Patients with esophageal disease and angina pectoris often perceive pain as originating from the same somatic fields. Another objective was to compare the effect of esophageal distension between animals with a non-inflamed or with an inflamed esophagus. For this study in anesthetized cats, we recorded extracellular action potentials from T2-T7 spinal neurons that responded to intraluminal distension of an untreated or a turpentine-inflamed distal esophagus. Threshold distension volumes were compared between these 2 groups of animals. Neurons also were examined for effects of intracardiac bradykinin injection and somatic stimuli. Results showed that spinal neurons responded to a smaller threshold distension volume when cells in animals with an inflamed distal esophagus were compared to cells in animals with a non-inflamed distal esophagus. Spinal neurons that received input from the distal esophagus also received convergent input from the heart and somatic fields. Our data supported the hypotheses that (1) referred pain from the distal esophagus resulted from activation of the same spinal neurons by visceral and somatic input, (2) pain originating from the distal esophagus and heart might be difficult to distinguish because of viscerosomatic and viscerovisceral convergence onto the same spinal neurons, and (3) an inflamed distal esophagus might be more sensitive to distension than a non-inflamed esophagus.
Afferent Pathways Animals