CHANGES IN ENTERIC NEURAL REGULATION OF SMOOTH-MUSCLE IN A RABBIT MODEL OF SMALL-INTESTINAL INFLAMMATION

In vitro electrophysiological studies of ileal circular muscle from ra bbits with ricin-induced inflammation tion were performed to investiga te whether altered neural control or myogenic activity contributes to previously described changes in in vivo myoelectric activity. Ricin tr eatment increased mean slow-wave amplitude but not frequency or restin g membrane potential. Prolonged electrical field stimulation evoked a hyperpolarization during the stimulus train and a depolarization on ce ssation of stimulation. In the presence of atropine, the depolarizatio n was larger in ricin-treated tissue than in control tissue, showing t hat ileitis enhanced noncholinergic excitation. The nitric oxide synth ase inhibitor N-nitro-L-arginine methyl ester reduced the hyperpolariz ation in ricin-treated but not in control tissue, suggesting that infl ammation increased nitric oxide-mediated inhibition. Substance P desen sitization reduced noncholinergic excitation and mean slow-wave amplit ude only in ricin-treated tissue, demonstrating that changes in these parameters during inflammation resulted from increased release of, or sensitivity to, tachykinins. These data suggest that acute ileitis alt ers tachykinin- and nitric oxide-mediated neurotransmission that may a ffect the normal pattern of ileal motility and/or sensory reflexes.