We investigated the effects of autonomic drugs and the role of intestinal contents on the motility changes that occur during acute obstruction. Myoelectric activity was recorded from seven electrodes spaced at 3-cm intervals along the midjejunum of nine 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 of obstruction failed to restore inhibited motor activity to control levels. Atropine sulfate (50 micrograms/kg) decreased and neostigmine (5 micrograms X kg-1 X 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. These results suggest that changes in luminal contents and in nervous activity both contribute to the intestinal motility changes that accompany obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)
A single strain gauge was implanted chronically in the proximal jejunum of the rat to record contractions. FAsted pentobarbital-anesthetized animals received glucagon, caerulein, or isotonic saline control infusions intravenously while contractions were recorded. In control animals, the distribution of contractions in time showed clusters, with peaks at intervals of 14.24 +/-5.6 (SD) min. Glucagon produced dose-related inhibition of contractions. Caerulein at two lower doses produced a more uniform distribution of contractions in time; a higher dose caused inhibition. In other fasted rats, an isotopically labeled bolus was given through a chronically implanted duodenal cathether, and its distribution along the small intestine was examined in animals receiving the same doses of glucagon, caerulein, and saline. Glucagon caused a dose-related delay in transit. Those doses of caerulein that produced a uniform distribution of contractions accelerated transit; the dose that inhibited contractions delayed transit. Doses of glucagon and caerulein known to affect both motility and transit did not significantly affect water movement. The fasted rat resembles the fasted go in respect to the temporal distributions of jejunal contractions at a single point. Both quantitative and qualitative changes in contractions induce changes in transit.
Gatorade and N-ORS seem to be as effective as Pedialyte in correcting dehydration and in improving bowel symptoms. All 3 solutions were safe. Unlike other groups, hypokalemia persisted in the Gatorade group. Gatorade and N-ORS may be effective in the treatment of dehydration associated with mild viral gastroenteritis.
The purpose of the study was to compare colonic motor patterns before and after a single abdominal dose of X-rays in dogs. Recordings were made from five serosally implanted strain gauges at equidistant intervals along the colon in seven dogs (2 dogs also had 2 jejunal electrodes and 1 had ileal electrodes). Control recordings were made for 3 h in the fasted state and daily for 2 wk after an absorbed X-ray dose of 938 cGy was delivered to the abdomen. The duration of migrating colonic motor complexes decreased from 7.2 +/- 0.5 to 3.9 +/- 0.4 min while the mean amplitude fell from 10.3 +/- 0.6 to 1.8 +/- 0.2 g (P < 0.05). The rate of nonmigrating colonic motor complex occurrence increased from 0.6 +/- 0.1 to 1.2 +/- 0.2 per hour (P < 0.05). Colonic giant migrating contractions were rarely observed during control recordings (2 in 80 h of recording). In contrast, repetitive clusters of giant contractions were observed 5-8 days after exposure in five of seven dogs (1.5/h) and were associated with restlessness, whining, and passage of diarrheal stools (sometimes bloody) with nearly every occurrence. The basic colonic motility patterns were less disrupted than were jejunal myoelectric patterns at the same irradiation dosage. However, the study demonstrates the important role of colonic giant migrating contractions in pathological diarrheal states such as irradiation injury.
The effect of the beta-adrenergic agonist isoproterenol on intestinal myoelectric activities was studied in fed dogs. A 15-min isoproterenol infusion (0.5 micrograms X kg-1 X min-1) initiated activity fronts after a meal in 14 of 16 experiments. The phase III motor activity was of similar duration and migrated aborally at the same rate as spontaneous fronts occurring in the interdigestive period; however, the activity fronts usually originated in the midjejunum and seldom migrated to the terminal ileum. The isoproterenol-induced fronts were blocked by pretreatment with propranolol (1 mg/kg). Activity fronts were not induced by sodium nitroprusside (10 micrograms X kg-1 X min-1), even though it inhibited myoelectric activity and induced hypotension and tachycardia to a degree similar to that caused by isoproterenol. The effects of isoproterenol were not blocked by vagotomy. Longer isoproterenol infusions of 2 h produced one but not more activity fronts and infusions in the fasted state did not induce premature fronts. These results do not support the hypothesis that the effect of isoproterenol is due to a neural reflex, and further studies are necessary to determine which of several potential mechanisms is responsible for this effect.
Seven female dogs (15-20 kg) were instrumented with seven bipolar electrodes sutured at 3-cm intervals to the serosal surface of the proximal jejunum and were exercised at different intensities and durations on a motor-driven treadmill. Slow-wave frequency increased (P less than 0.05) from preexercise control during prolonged (90 min) exercise and during recovery after short-term exercise (30 min) at 70% heart rate reserve (HRR). These changes were associated with an increase in core temperature. Spike-burst frequency (SBF) increased (P less than 0.05) with moderate exercise (50% HRR), but the magnitude was small. When exercise was extended beyond 30 min and during all recovery periods, SBF decreased significantly. Exercise produced migrating myoelectrical complexes in three experiments and less dramatic pattern changes characterized as "clustered contractions" (regular spike bursts preceded and followed by the absence of spike bursts) in at least nine other experiments. We conclude that exercise does alter jejunal myoelectrical activity, but myoelectrical patterns may be more important in explaining exercise-induced gastrointestinal symptoms than changes in spike-burst frequency or duration.
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