Determinants of intrabolus pressure during esophageal peristaltic bolus transport

Determinants of intrabolus pressure during esophageal peristaltic bolus transport JUNLONG REN, BENSON T. MASSEY, WYLIE J. DODDST, MARK K. KERN, JAMES G. BRASSEUR, REZA SHAKER, SANDRA S. HARRINGTON, WALTER J. HOGAN, AND RONALD C. ARNDORFER Departments of Radiology and Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin 53226; and Department of Mechanical Engineering, Pennsylvania State University, University Park, Pennsylvania 16802 Ren, Junlong, Benson T. Massey, Wylie J. Dodds, Mark K. Kern, James G. Brasseur, Reza Shaker, Sandra S. Harrington, Walter J. Hogan, and Ronald C. Arndorfer. Determinants of intrabolus pressureduring esophageal peristaltic bolus transport. Am. J. Physiol. 264 (Gastrointest. Liver physiol. 27): G407-G413, 1993.-Previous manometric studiesof esophagealfluid bolus transport in humanshave generally ignoredthe hydrodynamic distinction betweenintrabolus pressureand pressurewithin the lumen-occluded,contracting esophagealsegment. In this study we obtained concurrent esophagealvideofluoroscopic and intraluminal manometric recordings in supinenormal volunteers using different bolus volumes and viscosities and abdominal compression.Intrabolus pressureincreasedwith bolus volume, viscosity, and abdominal compression.Esophagealdiameter increasedwith larger bolus volumes,and this increasewas correlated with increasesin intrabolus pressure.Intrabolus pressurewas highest in the bolus tail. Peak intraluminal pressures>20 mmHg above basalintrabolus pressurealmost invariably were associatedwith effective peristalsis, whereas values of this pressure differential ~20 mmHg frequently were associatedwith ineffective peristalsis and retrogradebolus escape.Intrabolus pressurecan serveasan important indicator of the forces resistingperistaltic transport and the occurrenceof ineffective bolus transport. videofluoroscopy; videofluoromanometry; esophagealperistalsis; esophagealmanometry; lower esophagealsphincter EVALUATION of esophageal motility traditionally has focused on the peristaltic pressure waveform that results from the aborad sequence of esophageal muscle contraction and relaxation. Quantifiable characteristics of this waveform (e.g., amplitude, duration, and velocity) have been demonstrated previously to be affected by alterations in certain physical bolus parameters, such as volume (7, 10, 12, 16, 18) and viscosity (9), as well as by obstruction to esophageal outflow (8, 15). More recent analyses of the relationship between intraluminal manometric findings and peristaltic esophageal transport of a fluid bolus indicate the importance of considering separately the two pressure domains recorded by manometry: that within the fluid bolus and that within the esophageal segment whose lumen is occluded and devoid of bolus fluid as a result of esophageal contractions (2-4). Pressures within these two domains are distinct from one another and are not transmitted between domains when the esophageal lumen is completely sealed by the oncoming contraction wave (2). Although central to an understanding of the hydrodynamic forces that determine esophageal transport of a fluid bolus, the domain of intrabolus pressure has been largely neglected in most previous studies. The THE MANOMETRIC

7 Deceased 2 August 1992. 0193-1857/93

aim of this study was to evaluate how alterations in swallowed bolus variables and esophageal outflow obstruction could affect intrabolus pressure during peristaltic transport through the esophagus. In addition, the relationship between the two pressure domains when peristaltic bolus transport failed was assessed. The findings of this study were also used to validate the predictions of a fluid mechanical model of esophageal bolus transport regarding intrabolus pressure profiles (2-4). METHODS

Twenty-six healthy malesubjects[ages30.7 rf~8.0 (SD), range 23-50 yr] were studied with concurrent esophagealmanometry and videofluoroscopy, hereafter termed videofluoromanometry. The protocol was approved by the Human ResearchReview Committee of the Medical Collegeof Wisconsin. Subjectswere preselectedbasedon preliminary manometric studiesindicating both normal esophagealperistalsis and increasedintragastric pressureduring abdominal compression. For manometry two different catheters were used,eachmade from extruded multilumen polyvinyl tubing having an outer diameter of 4.5 mm. Each catheter had seven recording sites beginning 1 cm from its end and spacedevery 3 cm (catheter 1) or 1 cm (catheter 2). A tantalum marker placedadjacent to each recording orifice showedits location on videofluoroscopy. The catheters were infused with bubble-freewater at 0.5 ml/min by a pneumohydraulic capillary infusion pump (1). For eachstudy, one of the two catheters waspassedtransnasally and positioned so that the distalmost recording site was 1 cm proximal to the manometrically located lower esophagealsphincter. The subjects weresupinewhen studied,and the external pressuretransducerswere placed at the level of the midaxillary line to minimize hydrostatic effects. Manometric data were recorded on a polygraph (Sensormedics,Oxnard, CA) with eachchannel set at a full-scale deflection of 80 mmHg and a paper speedof 25 mm/s. Videofluoroscopy was recordedon 0.5-in. tape at 30 frames/s with a Super-VHS videocassetterecorder (model AG1960, Panasonic, Secaucus,NJ). A modified dual timer (Thalner Electronic Laboratories, Ann Arbor, MI) encoded time in hundredths of a secondon each video frame while sendinga pulse signalat l-s intervals to a channelon the polygraph tracing (11). Fluoroscopy time was limited to 3 min. During videofluoromanometry subjectsswalloweda standard low viscosity (150 cP/sp gravity 1.8) barium preparation (Liquid E-Z, E-Z-EM, Westbury, NY) and/or a high viscosity (63,000 cP/sp gravity, SG 2.9) barium preparation [made by mixing powdered E-Z-EM barium with Knott’s Berry Farm strawberry syrup (13)]. Bolus volumesof 2, 5, 10, or 20 ml were used in a random sequence.During someswallows,abdominal compressionwasapplied with a pressurecuff held in placeby a binder and inflated to a pressureof 90 mmHg. This producedan intragastric pressureof 20-30 mmHg, as determinedby briefly positioning the manometry catheter in the stomachat the start

$2.00 Copyright 0 1993 the American Physiological

Society

G407

G408

ESOPHAGEAL

INTRABOLUS

and end of each study. During somebarium swallowsthe fluoroscopeimageintensifier wasmovedover the length of the esophagussoasto keepthe tail of the barium bolus constantly in view. During other recording sequences,the image intensifier (g-in. magnification) was kept in a fixed position over either the proximal or the distal half of the esophagus.Becausefluoroscopy time waslimited, not all combinations of bolus volume, bolus viscosity, and intragastric pressurewere recorded in each subject. Baseline intrabolus pressure (PBASE) at a manometric recording site was measuredat the time when the recording site was located halfway betweenthe bolus head and bolus tail. For six subjects,intrabolus pressuremeasurementswere obtained, using catheter 2, during two to seven 5-ml low viscosity barium swallowsat the time when the most proximal recording site was located 0.5 cm distal to the tip of the bolus tail. Thus all manometric recording sites were located within the bolus at that time, allowing an intrabolus pressuredistribution to be determined. With useof both catheters, intrabolus pressurevaluesat adjacent manometric sites, spaced3 or 1 cm apart, were compared at times when both siteswere locatedwithin the bolusbut outsidethe region of the bolus tail. Transit time was measured as the time required for the bolus tail to passadjacent manometric recording sites, as observedon videofluoroscopy. Manometrically, transit time was taken as the time for the major upstroke of the pressurewave to move from one manometric site to the next. The duration of lower esophagealsphincter (LES) opening was also determined on videofluoroscopy. The maximal transverse esophagealdiameter was measuredat the level of each esophagealrecording site for complete peristaltic sequences.Pooled measurementsof esophagealdiameters vs. baseline intrabolus pressure for multiple barium swallowsin different subjectsat a site 4 cm from the LES were analyzed to ascertain the pressure-diameterrelationship in this region. The peak intraluminal pressure(PAMP) and duration of the peristaltic pressurewave weremeasuredat all manometric sites, although in somesubjectsPAMP wasnot always recordedaccurately becauseof signal-clipping. For each recording site the difference between PAMP and PnAsE wasmeasured.This pressuredifference wascorrelated with whether bolus clearancewas complete (i.e., the peristaltic contraction wave stripped all the

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barium from the lumen) or incomplete (i.e., retrogradeescapeof barium occurred or distal progressionof the peristaltic wave was arrested,thereby leaving barium within the lumen) at that site. Groups of data were analyzed by multiple analysisof variance (ANOVA), paired or unpaired Student’s t tests, and regression analysis, where appropriate. Averaged values in the text are given as meanst SE, unlessotherwise stated. RESULTS

As seen in Figs. 1 and 2, videofluoromanometry allowed the determination of whether a manometric site was recording from the domain of intrabolus pressure or the domain of the lumen-occluded segment devoid of bolus fluid. Thus, at a given instant in time, the esophagus could be divided into a bolus segment and a no-bolus segment. As the bolus was transported distally manometric sites recorded first from within the bolus and . subseregion. During quently from within the lumen-occluded effective bolus transport, pressures within one dom .ain appeared to be independent of those in, the other. As shown in Figs. 1 and 3, in the absence of abdominal compression P BASE exhibited little change as the bolus moved down the length of the esophagus and was transported through the relaxed LES. During abdominal compression, however, P BASE rose significantly in the distal esophagus as the bolus was pressed between the advancing perista .ltic contraction wave and . the LES, which was occluded by the high abdominal pressure (Figs. 2 and 4). During peristaltic sequences in which bolus clearance from the esophagus was complete, intrabolus pressure rose to a level just above that of abdominal pressure, resulting in LES opening and entry of barium into the stomach. During abdominal compression intrabolus pressures increased distally for all bolus volumes and viscosities tested. The axial pressure profile within the bolus at a specific instant when the bolus was located in the distal esophagus is depicted schematically in Fig. 5. Pressures were

Videofluoroscopy

Manometry

7.21 s

9.69s

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11.61s 11.61s LES Opening

m TIME in SECONDS

15

Fig. 1. Concurrent manometric and videofluoroscopic findings during effective peristaltic transport. After subject swallowed 20 ml of low viscosity barium (Ba SW) esophageal contraction wave was seen to transport barium bolus completely through esophagus without retrograde bolus escape at any point. Hatched area under each pressure recording indicates interval during which that recording site was within barium bolus. Upward arrow on each tracing indicates instant barium bolus tail passed recording site, and recording site was no longer recording from intrabolus pressure domain. Baseline intrabolus pressure (PnAsE) while bolus was in distal esophagus was -10 mmHg, with adjacent recording sites at any instant having similar levels of PnAsE (so long as recording sites were outside region of bolus tail). In contrast, adjacent recording sites located within lumen-occluded portion of esophagus tend to exhibit widely varying pressures at given instant. Horizontal bar indicates interval of lower esophageal sphincter (LES) opening, as determined by presence of barium within LES. UES, upper esophageal sphincter.

ESOPHAGEAL UES

cm

Manometty

INTRABOLUS

G409

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Fig. 2. Effective bolus transport during abdominal compression. Intragastric pressure (not shown) elicited by abdominal compression of 90 mmHg was 28 mmHg. In this example, lo-ml high viscosity barium bolus is completely transported through esophagus without retrograde escape. Associated finding is that peak intraluminal pressure (PAMP) exceeds PnAsE by >30 mmHg at each recording site. Note that as bolus moves distally with time PnAsE rises from - 12 mmHg in proximal esophagus to -28 mmHg in distal esophagus. Compared with findings in Fig. 1, abdominal compression causes slowing of peristaltic wave and bolus transport between distalmost recording sites.

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similar throughout most of the bolus length, except at the manometric site located in the region of the bolus tail. At this site, intrabolus pressure was significantly elevated above that of more distally located manometric sites. Similarly, when adjacent manometric recording sites were located within the bolus but outside the region of the bolus tail, these sites recorded an intrabolus pressure that was always within l-2 mmHg of each other. Intrabolus pressures at such adjacent recording sites were similar for all bolus volumes and viscosities tested as well as for all bolus locations within the esophagus and during abdominal compression.

The effects of bolus volume and viscosity on PBAsE are shown in Figs. 3 and 4. Increases in bolus volume were associated with increases in PBAsE. Similarly, PBAsE was higher with higher viscosity boluses but only for the larger lo- and 20-ml bolus volumes. In the distal esophagus the effects of bolus volume and viscosity on PnAsE were overshadowed by those of abdominal compression. There was good agreement between the transit times as determined by videofluoroscopy and manometry. For example, transit time from site 4 to site 1 (9 cm distance) for a 5-ml low viscosity bolus was 2.51 t 0.15 s when measured by videofluoroscopy and 2.61 t 0.16 s when measured by manometry. In the absence of abdominal

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Fig. 3. Effect of esophageal location, bolus volume, and bolus viscosity on PBAsE during effective bolus transport without abdominal compression. Recording sites are 3 cm apart. PBAsE was not significantly affected by esophageal location but was significantly higher with larger bolus volumes (P < 0.05). Increased viscosity caused significant (P < 0.05) additional increases in P BASE only for lo- and 20-ml bolus VOWumes. A: low viscosity (LV). B: high viscosity (HV).

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Fig. 4. Effect of abdominal compression on PnAsE during effective bolus transport. Abdominal compression was associated with significant (P < 0.05) increases in P BASE in distal esophagus for all bolus volume and viscosity combinations. Bolus volume and viscosity do not increase significantly P BASE distally at location 1, where PnAsE approaches intraabdominal pressure.

G410

ESOPHAGEAL

INTRABOLUS

compression transit time was similar throughout the esophagus and not significantly affected by bolus volume or viscosity (Fig. 6). However, with abdominal compression transit between distal sites 2 and 1 was significantly (P < 0.05) slowed for both high and low viscosity boluses. Increased bolus volume had an additional significant slowing effect at this level with high viscosity boluses only. In accord with the longer transit time, the duration of LES opening was significantly (P < 0.05) longer during

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Fig. 5. Schematic representation of axial distribution of intrabolus pressure during effective peristaltic transport of 5ml low viscosity barium bolus. Pressures were measured during 2-7 swallows in 6 subjects at instant when proximal manometric site (site 7) was determined on fluoroscopy to be 0.5 cm from tip of bolus tail. At this time bolus was in distal esophagus and esophageal emptying had not begun. Seven manometric sites are spaced 1 cm apart. Vertical dashed line indicates boundary between bolus-containing and lumen-occluded esophageal segments and is theoretically site of maximum intrabolus pressure (PM&. Intrabolus pressure at site 7, located in region of bolus tail that is contiguous to segment of actively contracting esophageal wall (vertical arrows), was significantly greater (P < 0.05) than that at other 6 sites, which were not significantly different from each other.

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Fig. 6. Effect of esophageal location, abdominal compression (AC = 90 mmHg: abdominal compression using a cuff pressure of 90 mmHg), and bolus volume and viscosity on transit time. A: LV, AC = 0 mmHg. B: HV, AC = 0 mmHg. C: LV, AC = 90 mmHg. D: HV, AC = 90 mmHg. By ANOVA transit time was not significantly affected by esophageal location when there was no abdominal compression. With abdominal compression transit time was significantly increased between sites 2 and 1. During abdominal compression, high viscosity combined with larger volumes to cause further increase in transittime at this distal location.

1 site

Esophageal Location Fig. 7. Effect of esophageal location, bolus volume, and abdominal compression on maximal intraluminal esophageal diameter during peristaltic transport of low viscosity barium boluses. A: AC = 0 mmHg. B: AC = 90 mmHg. ANOVA indicated that for most boluses, maximal esophageal diameter was greater in distal esophagus than that in proximal esophagus (P < 0.05) and was significantly (P < 0.05) greater with larger bolus volumes and abdominal compression.

abdominal compression. Increasing bolus volume, but not bolus viscosity, was also associated with a longer duration of LES opening. Abdominal compression also significantly (P < 0.05) prolonged the duration of the pressure wave in the distal esophagus, with larger bolus volumes having a further prolongation. Bolus viscosity did not affect the duration of the pressure wave. During effective bolus transport the maximum intraluminal esophageal diameter generally increased as the bolus moved distally (Fig. 7). Larger bolus volumes resulted in significantly (P < 0.05) larger diameters, as did abdominal compression. Bolus viscosity had no significant effect on esophageal diameter. As seen in Fig. 8, intrabolus pressure (in the region outside the bolus tail) was significantly correlated with maximal intraluminal esophageal diameter over the range of pressures and diameters studied. As shown in Fig. 9, in normal subjects peristalsis was on occasion ineffective, particularly when abdominal compression was applied. When esophageal muscular contractions were unable to occlude the lumen, PnAsE was typically of a magnitude close to that of the PAMP. The increment by which PAMP exceeded PBAsE was related to the effectiveness of peristaltic transport, as depicted in Fig. 10. Inspection of Fig. 10 indicates that a pressure differential of 520 mmHg is associated with a high probability of ineffective peristalsis with retrograde bolus escape. Ineffective peristalsis was more frequent in the distal esophagus. This relationship was found for all

ESOPHAGEAL

1’0

20

30

40

INTRABOLUS

50

lntrabolus Pressure (mmHg) Fig. 8. Relationship between intrabolus pressure and intraluminal esophageal diameter at manometric site 4 cm above LES. Data are shown for 20 swallows of 2-20 ml of LV or HV barium with AC = 0 mmHg or AC = 90 mmHg in 11 subjects. Number of data points exceeds 20 because several measurements were obtained for some swallows at different times in peristaltic sequence but only when manometric site was located within distal portion of bolus (i.e., outside tail region of bolus). Intrabolus pressure correlates significantly (r = 0.60, P c 0.05) with intraluminal esophageal diameter.

bolus volumes and viscosities tested and whether or not abdominal compression was applied. DISCUSSION

The findings of this study highlight the importance of reconsidering the paradigms by which esophageal manometric phenomena are interpreted. When evaluating the temporal variation in pressure at a manometric site during effective aborad peristaltic transport of a fluid bolus, one must recognize that the manometric site records first from within the bolus, then from within the lumen occluded region devoid of bolus fluid (2). As confirmed by the use of videofluoromanometry in this and previous studies (14, 17), the transition of the manometric recording site from the intrabolus pressure domain to the occluded lumen pressure domain is manifest by the pressure signal changing from an initial low-amplitude “plateau” cm above LES

Manometry 80

1

Bfsw

-

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G411

or “ramp” configuration to the “major upstroke” of the peristaltic wave, which has been the traditional focus of manometric analysis. Although the existence of the ramp pressure wave has been known for some time, including its modulation by bolus volume and esophageal outflow obstruction (ICI), this pressure wave subsequently has received little systematic study. Whereas the pressure profile at a manometric site within the lumen occluded esophageal segment is a direct reflection of the temporal variation in esophageal muscle contractile force at that site, the determinants of pressure within the bolus-filled region are hydrodynamically more complex (3). The pressure distribution within the bolus results from both the force generated by esophageal muscle contractions, which serves to propel the bolus, as well as the forces resisting bolus movement. Pressures within the lumen-occluded segment are not directly affected by forces that oppose bolus movement (2), which may explain the lack of consistent change in peak pressure amplitudes with changes in bolus viscosity (9) or outflow obstruction (8, 15, 17). However, factors producing resistive forces may indirectly affect pressure in the lumenoccluded region via m.echanisms that are not hydrodynamically determined. For instance, peak intraluminal pressure within the lumen-occluded region is affected by bolus volume (7,10,12,18), perhaps due to altered muscle preload (6) or neurogenic feedback. As was predicted from theoretica .l models of esophageal fluid bolus transport (2- 4), in this S tudy intrabolus pressure was found to be affected significantly by bolus volume and viscosity, as well as the resistance to esophageal outflow. The effects of these vari .ables were more pronounced in the distal esophagus, where the peristaltic contractions must compress the bolus and raise intrabolus pressure sufficiently to exceed intragastric pressure and so force open the relaxed lower esophageal sphincter if esophageal emptying is to occur (17). Indeed, several factors appear to limit the increase in intrabolus pressure Videofiuoroscopy

G412

ESOPHAGEAL

cm > LES:

19&16cm

1 13&10cm

1 7,4&lcm

INTRABOLUS

,

Esophageal Regions Fig. 10. Relationship between effectiveness of peristaltic bolus transport and difference between peak intraluminal pressure and baseline intrabolus pressure. Data are arrayed by esophageal location (sidehole position above LES in cm) and range of values for PAMP - PnAsE. E, number of sequences recorded at particular site and pressure differential in which peristalsis was effective; I, number of sequences with ineffective peristalsis. Shaded portion of circles represents proportion of sequences exhibiting effective peristalsis at that location and pressure differential.

in the setting of increased bolus volume, bolus viscosity, and/or outflow resistance. For one, the diameter of the esophagus increases with both bolus volume and intrabolus pressure, as shown in Figs. 7 and 8. Additionally, the bolus transit time increases with abdominal compression, as seen in Fig. 6. Abdominal compression also increases the duration of LES opening. These alterations in transit have been described previously (8, 9, 15, 17) and have been hypothesized to result from myogenic or neurogenic feedback. By reducing intrabolus pressure, such feedback could serve to decrease the stress in the distended esophageal wall. Although manometric analysis previously has emphasized the temporal variation in pressure at a fixed site, one can also evaluate the spatial distribution of pressure at specific times (5). This was accomplished in this study by using a manometric array with close spacing of recording sites and a consistently identifiable time (here determined by the position of the bolus tail relative to the proximal manometric recording site). As predicted by previous models (2, 3)) we found that within a moving fluid bolus the pressure profile along the bolus had small variations in the region outside of the bolus tail. This was the case whether the bolus was positioned proximally or distally within the esophagus. This relative uniformity of pressure within the majority of the bolus that is located distal to the bolus tail allowed the pressure at a location readily identifiable on videofluoroscopy (the axial center of the bolus) to be used as a reliable estimate of the intrabolus pressure throughout this region, which we term PBAsE. However, the pressure within the bolus tail, or closure segment, was significantly elevated above the more distal regions of the bolus. Theoretically, during peristaltic transport the maximum intrabolus pressure (PMAX) should occur at the tip of the bolus tail (4).

PRESSURE

For effective peristaltic bolus transport to occur, esophageal circular muscle contractions must be of sufficient magnitude to generate a PAMP that exceeds the PMAX, located at the tip of the bolus tail. It has been pointed out previously (2, 3) that retrograde bolus escape takes place when PAMP does not exceed PMAX. Although PMAX was not measured specifically in this study, we did find a relationship between the pressure differential PAMP PnAsE and the occurrence of ineffective peristalsis. Similar to the findings in the cat (17), when this pressure differential exceeded 20 mmHg at a manometric site, peristalsis was almost invariably effective and no bolus was left behind at that site. A pressure differential of ~20 mmHg, however, was associated with a high probability of ineffective peristalsis with retrograde bolus escape at that manometric site. Episodes of ineffective peristalsis were more likely to be found in the distal esophagus, the region where the highest P BASE values were observed in this study. Hence, in general PAMP must be higher in the distal esophagus to prevent ineffective peristalsis from occurring, consistent with previous findings (11). Because PnAsE varies little over the majority of the bolus length, comparison of the ramp or plateau of pressure at the onset of the peristaltic pressure complex to the peak pressure at a manometric site allows some prediction as to whether peristalsis was effective at that site. We conclude that the findings on videofluoromanometry during esophageal peristaltic bolus transport validate hydrodynamic models of this process. Intrabolus pressure is affected significantly by factors resisting bolus transport and, as such, has the POtential to be an important indicator of the presence of abnormal resistive forces. The relationship of intrabolus pressure to peak intraluminal pressure allows reliable prediction of effective peristalsis and can suggest the presence of ineffective peristalsis. Prevailing paradigms for esophageal manometry should be expanded so as to include the measurement of intrabolus pressure in future studies of esophageal bolus transport. The assistance of Candy Hofmann and Jan Staedler is appreciated. This study was supported by National Institutes of Health Grants ROl-DK-25731 and ROl-DC-00669 to W, J. Dodds, and ROl-DK-41436 to J. G. Brasseur, and by a grant (RR-00058) from the Clinical Research Center of the Medical College of Wisconsin. Preliminary findings were presented at the American Gastroenterological Association Annual Meeting, New Orleans, LA, May 1991, and abstracted in Gastroenterobgy 100: 486, 1991. Address for reprint requests: B. T. Massey, Div. of Gastroenterology, Medical College of Wisconsin, Froedtert Memorial Lutheran Hospital, 9200 West Wisconsin Ave., Milwaukee, WI 53226. Received 23 December 1991; accepted in final form 22 September 1992. REFERENCES Arndorfer, R. C., J. J. Stef, W. J. Dodds, J. H. Linehan, and W. J. Hogan. Improved infusion system for intraluminal esophageal manometry. Gmtroenterology 73: 23-27, 1977. 2. Brasseur, J. G. A fluid mechanical perspective on esophageal bolus transport. Dysphugia 2: 32-39, 1987. 3. Brasseur, J. G., and W. J. Dodds. Interpretation of intraluminal manometric measurements in terms of swallowing mechanics. Dysphczgia 6: 100-119, 1991. 4. Brasseur, J. G., W. J. Dodds, B. T. Massey, M. K. Kern, J. F. Helm, and P. J. Kahrilas. Esophageal pressure during peristaltic transport of a fluid bolus: distinction between intrabolus 1.

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and contractile-segment pressure domains (Abstract). Gustroenterology 96: 56, 1989. 5. Brasseur, J. G., M. Li, P.-Y. Hsieh, W. J. Dodds, and M. K. Kern. Computer simulations of esophageal transport integrated with concurrent videofluoroscopy and manometry (Abstract). Gastroenterology

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6. Cohen, S., and F. Green. The mechanics of esophageal muscle contraction. Evidence of an inotropic effect of gastrin. J. Clin. Invest. 7.

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Mittal, R. K., J. Ren, R. W. McCallum, H. A. Shaffer, Jr., and J. Sluss. Modulation of feline esophageal contractions by bolus volume and outflow obstruction. Am. J. Physiol. 258 (Gustrointest.

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Kahrilas, P. J., W. J. Dodds, and W. J. Hogan. Effect of peristaltic dysfunction on esophageal volume clearance. Gastroenterology

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8. Dodds, W. J., W. J. Hogan, E. T. Stewart, J. J. Stef, and R. C. Arndorfer. Effects of increased intra-abdominal pressure on esophageal peristalsis. J. Appl. Physiol. 37: 378-383, 1974. 9. Dooley, C. P., B. Schlossmacher, and J. E. Valenzeula. Effects of alterations in bolus viscosity on esophageal peristalsis in humans. Am. J. Physiol. 254 (Gastrointest. Liver Physiol. 17): G8-Gll, 1988. 10. Hollis, J. B., and D. 0. Castell. Effect of dry swallows and wet swallows of different volume on esophageal peristalsis. J. Appl. 11.

Kaye, M. D., and R. M. Wexler. Alteration of esophageal peristalsis by body position. Dig. Dis. Sci. 26: 897-901, 1981. 13. Li, M., J. G. Brasseur, M. K. Kern, and W. J. Dodds. Viscosity measurement of barium sulfate mixtures for use in motility studies of the pharynx and esophagus. Dysphugia 7: 17-30, 1992. 14. Massey, B. T., W. J. Dodds, J. F. Helm, J. G. Brasseur, and W. J. Hogan. Abnormal esophageal motility: comparison of radiographic and manometric findings. Gastroenterology 101: 344-

12.

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Dodds, W. J., W. J. Hogan, D. P. Reid, E. T. Stewart, and R. C. Arndorfer. A comparison between primary esophageal peristalsis following wet and dry swallows. J. Appl. Physiol. 35:

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Liver

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