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We correlated the electrical and contractile activities of the cricopharyngeus (CP) to better understand the function of the CP and the upper esophageal sphincter (UES). In 40 decerebrate cats, we recorded resting and active tension of the CP and CP force and electromyographic (EMG) activity simultaneously during electrical stimulation of the pharyngoesophageal (PE) nerve, esophageal distension, or swallowing. In six intact cats, the change in diameter of the UES during food swallows was determined in two planes using videofluoroscopy. We found that resting tension of the CP developed quickly with stretch, and the strain-energy function, y = 6.5e3.4(z-1), fit (r = 0.94 +/- 0.06) this relationship. Active tension peaked at 1.68 +/- 0.03 times resting length, which is greater than the maximum distension during swallowing. Activation and relaxation of the CP occurred in approximately 50 and 120 ms, respectively. PE nerve stimulation bilaterally caused a force equal to approximately 90% of the summed force generated by separate stimulation of each PE nerve. The magnitude of the EMG response of the contralateral CP was approximately 18% of the ipsilateral response to unilateral PE nerve stimulation. We conclude that the CP exhibits tension throughout its physiological range of stretch. The CP functions more like a bilateral than a single contiguous muscle, and more like cardiac than striated muscle with regard to its passive elastic properties.

Previous manometric studies of esophageal fluid bolus transport in humans have generally ignored the hydrodynamic distinction between intrabolus pressure and pressure within the lumen-occluded, contracting esophageal segment. In this study we obtained concurrent esophageal videofluoroscopic and intraluminal manometric recordings in supine normal volunteers using different bolus volumes and viscosities and abdominal compression. Intrabolus pressure increased with bolus volume, viscosity, and abdominal compression. Esophageal diameter increased with larger bolus volumes, and this increase was correlated with increases in intrabolus pressure. Intrabolus pressure was highest in the bolus tail. Peak intraluminal pressures > 20 mmHg above basal intrabolus pressure almost invariably were associated with effective peristalsis, whereas values of this pressure differential < 20 mmHg frequently were associated with ineffective peristalsis and retrograde bolus escape. Intrabolus pressure can serve as an important indicator of the forces resisting peristaltic transport and the occurrence of ineffective bolus transport.

In conscious opossums, we evaluated the relationship between hepatic bile flow and the intestinal motor function during fasting as well as after feeding. In six opossums, bipolar electrodes were implanted from the gastric antrum to the terminal ileum. After cholecystectomy, the common duct was ligated, and a catheter was tied into the proximal common duct for collecting hepatic bile. During subsequent studies, hepatic bile flow was measured, and bile was returned to the duodenum through an externalized duodenal catheter. Cyclic increases in bile flow during fasting did not show a close correlate with the duodenal migratory motor complex (MMC) cycle. Rather, bile flow showed peak values [0.11 +/- 0.02 (SE) ml/min] when phase III MMC activity reached the midileum. Hepatic bile flow correlated closely with the amount of bile acid secreted by the liver. When the bile acid pool was depleted by diverting bile from the intestine, hepatic secretion of bile fell to uniformly low values of approximately 0.04 ml/min that did not show cyclic variation. Hepatic bile flow after feeding increased to a maximal value of 0.12 +/- 0.01 ml/min at 90 min. We conclude that increases in hepatic bile flow during fasting and after meals are determined mainly by variations in intestinal motor activity that alter small bowel transit and thereby affect the enterohepatic circulation of bile acids.

Our goals in this study were to evaluate the mechanisms operative in swallow-associated opening of the upper esophageal sphincter (UES) and to determine the dynamics of fluid flow across the sphincter. For this purpose, we obtained concurrent videofluorographic and manometric studies of 2- to 30-ml barium swallows in 15 normal subjects. We found that the resting UES high-pressure zone corresponded closely with the location of the cricopharyngeus. The findings indicated that manometric UES relaxation and anterior hyoid traction on the larynx invariably preceded UES opening. With graded increases in bolus volume, progressive increases occurred in UES diameter, cross-sectional area, flow duration, and transsphincteric flow rate. Intrabolus pressure upstream to the UES and within the UES at its opening during transsphincteric flow of barium remained within a narrow physiological range of less than 10 mmHg up to a bolus volume of 10 ml. With increases in bolus volume, anterior hyoid movement, UES relaxation, and UES opening occurred sooner in the swallow sequence to accommodate the early entry of large boluses into the pharynx. We conclude that during swallowing 1) normal UES opening involves sphincter relaxation, anterior laryngeal traction, and intrabolus pressure, 2) volume-dependent adaptive changes in UES dimension accommodate large bolus volumes and flow rates with minimal requirement for increases in upstream, or intrasphincteric, intrabolus pressure or UES opening duration, and 3) volume-dependent changes in UES dimensions as well as timing of UES relaxation and opening indicate a sensory feedback mechanism that modulates some components of the swallow response generated by the brain stem swallow centers.

We used an in vivo feline model to study striated and smooth-muscle esophageal responses to cervical vagal stimulation (VS). Circular esophageal contractions were measured by intraluminal pressure sensors and longitudinal contractions by a force transducer. Responses to VS were recorded before and after giving succinylcholine, atropine, or both. Circular contractions characteristic of striated and smooth muscle were recorded from the mid- and distal esophagus, respectively. With increases in VS frequency, the striated muscle showed rapid, repetitive twitches progressing to tetany. These fast contractions had a square-wave configuration at VS greater than or equal to 10 Hz and were abolished by succinylcholine. In contrast, the slow-twitch circular responses of smooth muscle showed no repetitive twitches and had a bell-shaped configuration. Two types of circular smooth-muscle contractions were observed: 1) A wave "on contractions" occurred 0.5-1.0 s after VS onset, regardless of stimulus length, and 2) infrequent B wave "off contractions" occurred only after stimulus cessation. The longitudinal esophageal contractions had a compound wave form with both striated and smooth-muscle components. Atropine abolished the slow component of the longitudinal contraction, the circular A wave, and peristalsis in the distal esophagus. We conclude that cholinergic motor neurons are an important pathway for eliciting peristalsis in feline esophageal smooth muscle.

In this study, we evaluated the effect of histamine on phasic contractile activity in the opossum sphincter of Oddi (SO). SO manometry was done in 35 animals, using an infused catheter system with minimal compliance. In anesthetized animals, phasic SO contractions occurred at a frequency of 7.3 +/- 0.3 (SE) contractions/min with an amplitude of 83 +/- 4 mmHg. Intravenous histamine (5-80 micrograms/kg) invariably inhibited the frequency and amplitude of SO phasic contractions. At larger doses, the SO contractions were abolished for several minutes. The SO inhibitory effect of histamine was duplicated by the selective H1-agonist, 2-pyridylethylamine, and abolished by H1-blockade with pyrilamine or neural blockade with tetrodotoxin. After tetrodotoxin, histamine and 2-pyridylethylamine caused an increased frequency and amplitude of SO contractions. This excitatory effect was blocked by pyrilamine. The histamine effects on SO phasic contractions were not altered by metiamide, atropine, phentolamine, propranolol, hexamethonium, or a large dose of nicotine. We conclude that 1) histamine depresses phasic SO contractions in the opossum; 2) histamine's depressant SO effect is mediated by H1 stimulation of noncholinergic, nonadrenergic SO inhibitory nerves, overriding an H1 stimulatory effect on SO smooth muscle; and 3) histamine has no H2-mediated effect on the opossum SO.

We studied the effect of motilin on myoelectric activity of the sphincter of Oddi (SO) and upper gastrointestinal tract in conscious opposums. In 17 animals, bipolar electrodes were implanted on the gastric antrum, SO, duodenum, and jejunum. Subsequent 8-h recordings reconfirmed our previous findings that SO spike burst rate changed with interdigestive cycles of the gastrointestinal migrating myoelectric complex (MMC), becoming maximal during passage of phase III activity through the duodenum. In eight animals, peak motilin levels were shown to occur concurrently with maximal SO spike burst rate and MMC phase III activity in the duodenum. Motilin infusion (0.3 and 0.9 micrograms X kg-1 X h-1), given for 30-60 min starting 10 min after duodenal phase III, elicited premature MMC activity that originated in the stomach. Maximal SO activity occurred coincident with passage of premature phase III activity through the duodenum. Pulse intravenous doses of motilin (25-1,600 ng/kg) generally caused an immediate increase in spike burst activity in the gastric antrum, duodenum, and SO that lasted 3-5 min and was often followed by a premature MMC, usually starting in the antrum and progressing through the duodenum and jejunum. Increases in SO spike burst rate also occurred concurrent with motilin-induced, premature duodenal phase III. Motilin given at 5-60% of the duodenal MMC cycle length elicited premature MMCs at 10-60% of the cycle, but no premature MMCs were elicited by any of the motilin doses at the 5% intervals.(ABSTRACT TRUNCATED AT 250 WORDS)

Our aim in this study is to determine whether extrinsic autonomic nerves regulated spike-burst rate in the opossum sphincter of Oddi (SO) during fasting or after feeding. We implanted electrodes on the distal SO, proximal SO, gastric antrum, duodenum, and jejunum of 20 animals. A cut transection and reanastomosis was done at different levels of the SO to interrupt putative extrinsic or intrinsic nerves, or the SO was painted with phenol to impair extrinsic nerves. Like controls, animals with a cut and reanastomosis at the proximal SO or at the SO-duodenal junction showed a normal fasting pattern of cyclic changes in SO spike-burst rate. In contrast, animals treated by a distal SO cut or phenol treatment at the distal SO lost the normal cyclic pattern of SO spike bursts and had a constant rate of approximately 4/min. A cut through the middle SO uncoupled the spike bursts in the proximal and distal SO. After feeding, all animals developed an SO spike-burst rate of 5-6/min that lasted for several hours. We conclude that the normal fasting pattern of SO spike bursts is regulated by extrinsic nerves that ascend cephalad along the sphincter segment, whereas the sustained increase in SO spike-burst rate after feeding is at least in part hormonal.