Colorectal distension as a noxious visceral stimulus: physiologic and pharmacologic characterization of...

This report presents evidence that colorectal distension is a reproducible, reliable, valid, noxious visceral stimulus that can be used in studies performed in awake, unanesthetized, unrestrained rats. Colorectal distension produces aversive behavior and cardiovascular and visceromotor responses which are quantifiable, reliable, reproducible and useful for inter- and intra-animal studies. The cardiovascular response, a pressor response with tachycardia, is graded and thought to be due to an increase in sympathetic outflow coupled with removal of vagal tone since it is attenuated in a dose-dependent way by atropine, propranolol, phentolamine, chlorisondamine and adrenal demedullation. The visceromotor response is a contraction of abdominal and hindlimb musculature. The distending pressure threshold for the visceromotor response (22.4 +/- 0.9 mm Hg) is significantly greater than that necessary to evoke a non-nociceptive response, relaxation of the anal sphincters (13.2 +/- 0.7 mm Hg). Both the cardiovascular and visceromotor responses act via brainstem loops since both are vigorous in decerebrate (midcollicular) but not spinalized (C1 or T6) rats. Anesthetics attenuated (alphaxalone/alphadolone, ketamine) or reversed (urethane, pentobarbital, alpha-chloralose) the cardiovascular responses to colorectal distension and attenuated (alphaxalone/alphadolone) or abolished (others listed above) the visceromotor response. Both morphine (systemic and intrathecal) and clonidine (intrathecal) produced a dose-dependent inhibition of both the cardiovascular and visceromotor responses to colorectal distension. Thus, in the awake, unrestrained rat, the cardiovascular and visceromotor responses to colorectal distension are quantifiable, reliable and reproducible signs of acute visceral nociception.