ABSTRACT
The physiology of visceral nociception has traditionally been elucidated by the examination of responses to ephemeral stimuli, such as the rapid distension of a viscus. However, it is now appreciated that such physiological studies are of only limited relevance to clinical pain, a situation in which the adaptive responses of a dynamic nervous system profoundly influence the processing of sensory traffic, clinically manifested by the appearance of allodynia and hyperalgesia (1). The effects of tissue injury and the subsequent inflammatory response are critical in determining the functional status of the sensory nervous system so that pain continues to be perceived long after a transient noxious stimulus has ceased. Therefore, the pathophysiology of visceral pain must be reexamined in models that incorporate a significant tissue injury and inflammatory components, so that the findings might be clinically relevant.
