Mechanisms of motility changes during acute intestinal obstruction in the dog

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Abstract
The effects of autonomic drugs and the role of intestinal contents on the motility changes that occur during acute obstruction were investigated. Myoelectric activity was recorded from 7 electrodes spaced at 3-cm intervals along the midjejunum of 9 conscious dogs. Another animal had electrodes evenly placed throughout the small bowel. Obstruction was created by inflation of an intraluminal balloon. Systemic arterial blood pressure and pulse rate were monitored. Initially, motor activity of the small intestine increased proximal to an acute intestinal obstruction and decreased distally. Recordings from the entire small intestine revealed that these effects occurred almost immediately in the region of the obstruction but not at more distant sites. Within 2-3 h, however, proximal hypermotility had extended to the duodenum and distal inhibition had progressed to the terminal ileum. Diversion of intestinal contents without obstruction reduced myoelectric activity distal to the site of drainage. However, reinfusion of chyme distal to the site obstruction failed to restore inhibited motor activity to control levels. Atropine sulfate (50 .mu.g/kg) decreased and neostigmine (5 .mu.g .cntdot. kg-1 .cntdot. min-1) potentiated the hyperactivity proximal to the obstruction, but neither agent significantly affected the distal inhibition. Phentolamine (1 mg/kg) and propranolol (1 mg/kg) had no effect on proximal or distal motor activity during obstruction; these were doses that blocked cardiovascular responses to adrenergic agonists. Changes in luminal contents and in nervous activity both apparently contribute to the intestinal motility changes that accompany obstruction. Increased motor activity proximal to an obstruction appears to be mediated by cholinergic nerves. Some of the distal inhibition of spike bursts may be mediated by noncholinergic, nonadrenergic pathways and some is the result of diminished intraluminal contents.