We studied the mechanisms of initiation and pathways for the propagation of intestino-intestinal inhibitory reflexes induced by close intraarterial injections of neostigmine in conscious dogs. Two or three T-shaped catheters were surgically implanted in the intestinal branches of the superior mesenteric artery to inject pharmacologic agents locally in 10-15-cm-long segments. Migrating myoelectric complexes were recorded by a set of 10 electrodes and straingauge transducers. Close intraarterial injection of neostigmine initiated strong contractions of long duration in the perfused segment that terminated phase III activity in progress 90-150 cm distal or proximal to the cannulated sites and stopped its further migration. Atropine or 4-diphenylmethoxyN-methylpiperidine methiodide injected just before neostigmine administration through the same catheter blocked both the local contractile effects and the reflex inhibition of phase III activity. Pirenzepine or hexamethonium injected in a similar manner did not affect the local response to neostigmine but blocked the reflex inhibition of phase III activity. A transection and reanastomosis in the mid-small intestine blocked the reflex inhibition by close intraarterial injection of neostigmine beyond the transection site. Pirenzepine, atropine, or hexamethonium injected through a middle catheter also blocked the reflex inhibition of phase III activity beyond the site perfused with these cholinergic antagonists. Close intraarterial administration of 4-diphenylmethoxy-N-methylpiperidine methiodide at a middle site had no effect on reflex inhibition. We concluded that strong spasmodic contractions in the small intestine initiate an intestino-intestinal inhibitory reflex in both directions. This reflex is mediated through an intrinsic neural pathway involving nicotinic and M1 muscarinic receptors.
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