Changes in enteric neural regulation of smooth muscle in a rabbit model of
small intestinal inflammation.
Goldhill, J. M., K. M. Sanders, R. Sjogren & T. Shea-Donohue.
Department of Medicine, USUHS, Bethesda, MD 20814-4799, Department of
Physiology, University of Nevada School of Medicine, Reno, NV, 89557,
Gastroenterology Service, Kaiser Permanente, 201 North Washington Street,
Falls Church, VA, 22046
APStracts 2:0009G, 1995.
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, contribute 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 upon cessation of stimulation. In the presence of
atropine, the depolarization was larger in ricin-treated tissue than
controls, showing that ileitis enhanced non-cholinergic excitation. The
nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester, reduced the
hyperpolarization in ricin-treated but not control tissue, suggesting that
inflammation increased nitric oxide-mediated inhibition. Substance P
desensitization reduced non-cholinergic 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 which may affect the
normal pattern of ileal motility and/or sensory reflexes.
Received 7 April 1994; accepted in final form 10 January 1995.
APS Manuscript Number G129-4.
Article publication pending Am. J. Physiol. (Gastrointest. Liver Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 February 1995.