Intermittent ischemia may play an important role in the pathogenesis of inflammatory bowel diseases. An experimental model of neuronal ischemia was used to study the effect of anoxia, hypoglycemia and ischemia on neuro-effector transmission in guinea pig ileum and to investigate the possibility that nitric oxide might be involved in producing deficits in neuro-effector transmission after ischemia. Depression of cholinergic neuro-effecror transmission induced by anoxia were apparent shortly and were reversible rapidly. The maximum inhibition was 90% and it was suggested to be prejunctional. Non-cholinergic neuro-effector contractions were inhibited by the same percent by anoxia but the recovery was incomplete and slower compared to cholinergic contracrions. were inhibited by the same percent by anoxia but the recovery was incomplete and slower compared to Cholinergic contractions. Glucose-free solutions also, induced a reversible failure of cholinergic neuro-effecror transmission bur of slow onset. Nitric oxide synthesis inhibitor, N-nitro-l--arginine methvl esrer hvdro- chloride (L—NAME) failed to prorecr neuro-effecror transmission against ischemia insults. Thus, it is concluded that any disruption in intestinal activity with any patholoqical conditions associated with intesrinal ischemia may result from disturbance in the function of enteric neurons. This disruption was nor due to cessation of neuronal function or neuronal cell death, since the effects were so readily and completely reversible. The deficits in neuro-effecror transmission produced by ischemia in the gut did nor appear to involve nitric oxide production since inhibitors of nitric oxide synthesis provided no protection against ischemic insults.
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