In the present study, effects of ileal infusions of nutrients on motor patterns of the proximal small intestine and on gastric emptying were investigated in dogs. An acaloric meal was administered orally, and equicaloric loads of amino acids, oleate, and glucose were infused into the ileum at different doses (0.3, 0.6, and 0.9 kJ/min). The computerized analysis of motor patterns was focused on the differentiation between stationary and propagated contractions recorded by closely spaced extraluminal strain gauges. All three nutrients exerted inhibitory effects on gastric emptying and on contraction force and frequency of the proximal small intestine. Additionally, the propulsive motor pattern induced by the acaloric meal was modulated by reducing the number of contraction waves and their length of spread. All the effects were dose dependent. Among the three nutrients, glucose significantly changed motility at lower doses compared with amino acids and oleate. We conclude that in dogs the ileal brake mechanism is induced by all three nutrients and that it influences not only contraction force and frequency but also the motor patterns of the proximal small intestine.
The aim of the study was to clarify the effects of hypertonic solutions on jejunal motility. The study focused on differential effects of hypertonic saline and nutrients. Motility of the canine proximal jejunum was recorded with closely spaced strain-gauge transducers. During fasting, hyperosmotic solutions (up to 1520 mosmol/liter) of saline or nutrients (1 kcal/ml) were infused into the proximal jejunum (0.5-1.5 ml/min) up to 6 hr. The hyperosmotic solutions stimulated jejunal motility. With both increasing osmolarity of saline or increasing energy load of nutrients, jejunal motility linearly declined. The reduction of motility was associated with a change in motor pattern from a propulsive to a more segmenting one. Hypertonic glucose evoked a significantly smaller level of motor activity compared with both saline (at given osmolarities) and an elemental diet (at given energy loads). Motility parameters were not different between glucose and maltose, although osmolarity of maltose was less than half (760 vs 1520 mosmol/liter). In contrast, a mixture of glucose-fructose exerted a smaller inhibition of jejunal motility than glucose. The hypertonic solutions of saline or nutrients were tolerated over 2 hr; with hypertonic saline retrograde power contractions with or without vomiting occurred, whereas with hypertonic nutrients vomiting was preceded by strong inhibition of jejunal motility. Three conclusions can be derived from the present results: (1) The behavior of jejunal motility suggested that the motor activity was the result of both a local stimulation and an inhibitory feedback mechanism. (2) The different degree of inhibition between glucose and saline indicated that the nutrient itself played a major role in the inhibitory feedback regulation, whereas osmolarity was of minor importance. (3) Comparisons between different nutrients suggested a linkage between inhibitory control of motility and the absorptive capacity of the gut for the single nutrient.
This study was performed to clarify in detail the behavior of the propagation velocities and frequencies of contractions along the canine small intestine. In conscious dogs, duodenal, jejunal, and ileal contractions were recorded by multiple, closely spaced strain gauges and analyzed by a computerized method. During both the interdigestive and postprandial states, the propagation velocity increased from the duodenal bulb to the distal duodenum and declined aborally within the jejunum, reaching rather constant values in the ileum. The decrease was steepest in the proximal part of the jejunum. In contrast to the propagation velocities, the contraction frequencies were almost constant in the upper small intestine. In the ileum, the contraction frequencies were markedly lower than in the upper small intestine, indicating that the aboral decrease in frequency occurred in the distal parts of the jejunum. We conclude that both the propagation velocities and the frequencies of contractions decline aborally in a nonlinear fashion. However, the nonlinear patterns of the frequency and the propagation velocity gradients are different.
The motor pattern of the phase I1 of the migration motor complex ( M M C ) is poorly characterized and it remains t o be determined whether it differs from the fed motor-pattern. Furthermore, discrepancy exists on the disruption of ongoing M M C s b y feeding, and finally, the understanding of the behaviour of phase IIIs during enteral nutrition is incomplete. Therefore, canine intestinal motility was studied after meal and during enteral infusion o f nutrients (elemental diet, glucose, maltose, amino acids) or of hypertonic saline (300-1520 mosmol kg-I). Motility o f the proximal, mid-and distal jejunum was recorded with straingauge transducers. The motor patterns o f the interdigestive phase I I , after feeding and during enteral nutrition were ana1.vsed b y a computer. Additionally, the disruption of the M M C by food and b y enteral infusion of nutrients or hypertonic saline was investigated. The interdigestive phase I I consisted of three different contractile patterns, clustered contractions, a mixed contractile pattern and non-migrating bursts o f propagated contractions (NBPCs). NBPCs differed significantly from the phase I I I activity in several motility parameters and b y the lack o f aboral migration. Only small differences existed between the motor patterns of phase I1 and o f the fed state, whereas the motor pattern induced b y enteral infusion of an elemental diet differed significantly from that of phase I I . Ongoing M M C s o f the proximal jejunum often continued to migrate to the mid-and distal jejunum. During enteral infusion of nutrients or of hypertonic saline, phase Ills recurred. The migration o f ongoing phase Ills and the recurrence o f subsequent phase Ills decreased with increasing caloric or osmotic loads. The following conclusions were reached. (a) The phase I I of the M M C is a complex motor-pattern. N B P C s represent a n e w contractile pat-tern. (b) The M M C is a characteristic feature of the empty gut. After meal and during enteral nutrition, phase IIIs are usually suppressed but they can recur during the digestive period.
Little is known on the effects of enteral nutrition on intestinal motor patterns. In dogs, intestinal motility was recorded with multiple extra-luminal strain-gauges. A n elemental diet was infused into the jejunum (0.5-2.5 kcal min-') over 6 h. The elemental diet or dog food were also administered orally for comparison. Iejunal infusion o f the elemental diet stimulated jejunal motility; the motor pattern was characterized by clustered contractions. During enteral feeding, stimulation of jejunal motility was initially less (lower motility index, lower incidence of contraction waves and shorter spread of contractions) compared with oral feeding. Iejunal motility declined linearly with time, the decline being less profound during enteral than after oral feeding. Linear correlations also existed between motility parameters and energy loads; increasing energy loads produced reduction instead of enhancement of motility. Strong inhibition of motility followed by vomiting occurred with energy loads 2 2 kcal min-'. The following conclusions were reached: (a) jejunal feeding evoked different patterns of jejunal motility compared with oral feeding; (b) jejunal motility was the result of both a local stimulation and an inhibitory feedback mechanism; (c) intestinal overload of nutrients was indicated bymarked inhibition of motility. These results indicate that recording of motility during enteral nutrition might be a useful diagnostic tool for predicting gastrointestinal sequelae.
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