AJP - Gastrointestinal and Liver Physiology, Vol 268, Issue 5 823-G830, Copyright © 1995 by American Physiological Society

ARTICLES

Changes in enteric neural regulation of smooth muscle in a rabbit model of small intestinal inflammation

J. M. Goldhill, K. M. Sanders, R. Sjogren and T. Shea-Donohue
Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799, USA.

In vitro electrophysiological studies of ileal circular muscle from rabbits with ricin-induced inflammation were performed to investigate whether altered neural control or myogenic activity contributes to previously described changes in in vivo myoelectric activity. Ricin treatment increased mean slow-wave amplitude but not frequency or resting membrane potential. Prolonged electrical field stimulation evoked a hyperpolarization during the stimulus train and a depolarization on cessation of stimulation. In the presence of atropine, the depolarization was larger in ricin-treated tissue than in control tissue, showing that ileitis enhanced noncholinergic excitation. The nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester reduced the hyperpolarization in ricin-treated but not in control tissue, suggesting that inflammation increased nitric oxide-mediated inhibition. Substance P desensitization reduced noncholinergic excitation and mean slow-wave amplitude 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 alters tachykinin- and nitric oxide-mediated neurotransmission that may affect the normal pattern of ileal motility and/or sensory reflexes.

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