UPPER ESOPHAGEAL RESPONSES TO INTRALUMINAL DISTENTION IN MAN

Transcription

1 GASTROENTEROLOGY 72: , 1977 Copyright 1977 by the American Gastroenterological Association Vol. 72, No.6 Printed in U.SA. UPPER ESOPHAGEAL RESPONSES TO NTRALUMNAL DSTENTON N MAN D. R. ENZMANN, M.D., G. S. HARELL, M.D., AND F. F. ZBORALSKE, M.D. Department of Radiology, Stanford University School of Medicine, Stanford, California This investigation determined the site(s) of elicitation and origin of secondary peristalsis in the human esophagus and characterized the upper esophageal sphincter (UES) and proximal esophageal body responses accompanying intraluminal distention. n 7 normal persons, an intraluminal transducer probe manometrically recorded the UES and 5- and O-cm levels of the esophageal body. A second probe with a balloon attached 2 cm above the proximal strain gauge was located so that the balloon was 3 and 4 cm below the UES and 4 distentions were done. The balloon probe was moved in 2-cm increments (four distensions at each site) until lower esophageal sphincter pressures were recorded. No secondary peristalsis occurred after distention in the proximal 6 cm. The incidence of secondary peristalsis increased as the distention site moved distally. Sixty-nine per cent of secondary peristaltic waves originated in the esophageal body proximal to the distention site. The UES pressure significantly increased over resting pressure (augmentation) during 63% of distentions. The esophagus proximal to the balloon and below the UES usually responded to distention with augmentation. Augmentation of the UES and proximal esophageal body in response to esophageal intraluminal distention and the resultant initiation of secondary peristalsis above the distention site comprise a highly integrated pressure barrier to esophagopharyngeal reflux. Contradictory statements exist regarding the esophageal responses to intraluminal distention. The characteristics of secondary peristalsis and the response of the upper esophageal sphincter (UES) and esophageal body proximal to the site of distention have all been debated. 2-8 Understanding the secondary peristaltic, UES, and proximal esophageal body responses to intraluminal distention in human beings is important as they represent the esophageal defense mechanisms against esophagopharyngeal reflux. This investigation characterizes the normal physiology of these three responses to intraluminal balloon distention in the proximal twothirds of the human esophagus. Materials and Methods Seven normal volunteers (6 males and 1 female), aged 19 to 33, were studied. nformed written consent was obtained from all. The research protocol was approved by the Medical Subcommittee of the Committee on the Use of Human Subjects in Received September 23, Accepted December 20, An abstract of this work has been published. 1 Address requests for reprints to: F. Frank Zboralske, M.D., Department of Radiology, Stanford University School of Medicine, Stanford, California This study was supported in part by Grants GM 1707 from the National nstitute of General Medical Sciences, and AM from the National nstitute of Arthritis and Metabolic Disease, National nstitutes of Health, United States Public Health Service. Dr. Enzmann is an Academic Trainee in Diagnostic Radiology. His work is supported by Grant GM 1707 from the National nstitute of General Medical Sciences, National nstitutes of Health, United States Public Health Service Research of the Stanford University School of Medicine. Each volunteer had normal esophageal function as determined by history and esophageal manometry. Two intraluminal subminiature strain gauge pressure probes (model 31 probe, Honeywell Biomedical, Denver, Colo.) were used. Each transducer probe had three strain gauges, positioned 5 cm apart, which had a frequency response rated by the vendor as flat to about 5000 Hz. A pediatric endotracheal cuff balloon was attached to one probe so that the balloon center was 2 cm proximal to the upper strain gauge sensor (this assembly was termed the balloon probe). A tube was attached to the balloon for inflation via a 25 cc syringe. nflation volumes of 3 to 15 cc resulted in external balloon dimensions of 1.5 by 2.0 cm to 2.5 by 3.0 cm (width by length). Each pressure probe was connected to a Sanborn C carrier preamplifier and 7700 series polygraph (Sanborn Company, Waltham, Mass.) calibrated before and after each study. Both probes were passed through the nose into the stomach in 5 subjects; in 2 subjects, the nonballoon probe was passed through the mouth. The nonballoon probe was withdrawn at 1- cm increments from the stomach until the lower esophageal sphincter (LES) was localized and its distance from the nares or teeth measured. The probe was then withdrawn further until the UES was localized, noting its distance from the nares or teeth. Esophageal body length was calculated. This probe was then permanently positioned with the proximal recording tip in the UES, placing the other sensors at the 5- and 10-cm levels of the esophageal body. The balloon probe was similarly withdrawn at 1-cm increments to localize the LES. The LES measurements from both probes permitted accurate positioning of one probe in relation to the other. Each subject had one pneumograph attached around the neck and another around the chest to record deglutition and respirations, respectively. Each volunteer was studied in both the supine and sitting positions to assess whether position played a significant role in

2 June 1977 ESOPHAGEAL RESPONSES TO NTRALUMNAL DSTENTON 1293 these experiments; the starting position of the subjects was alternated between sitting and supine. The 3 and 4-cm esophageal body level (station 1) was the frrst distention site (fig. la). Subsequent stations were placed 2-cm increments distally. The most distal distention site was the 15 and 16-cm esophageal body level (station 7). This level placed at least two recording tips ofthe balloon probe in the esophagus permitting peristalsis determination in all but subject 6 (fig. lb). A gag response during balloon distention precluded testing the 1 and 2-cm level in all subjects. Test inflations of3- to 5-sec duration were performed at each station in all subjects before data collection was begun to establish the balloon distention volume which was just below the subject's threshold of discomfort for each study station. This individually determined distention volume for each station was used during the investigation. Data were analyzed from four technically acceptable 3- to 5-sec distentions (no deglutition during balloon inflation or within 15 sec after balloon deflation) at each station. The range of distending volumes for each station was: no. 1 (3 to 7 cc), no. 2 (4 to 8 cc), no. 3 (4 to 10 cc), no. 4 (4 to 11 cc), no. 5 (5 to 15 cc), no. 6 (6 to 14 cc), no. 7 (6 to 14 cc). Determinations could not be made in subject 5 at the 3 and 4-cm level in either position, in subject 6 at the 3 and 4-cm level in the sitting position, and in subject 4 at or above the 5 and 6-cm level in either position because distentions evoked a gag response. A 30-sec interval was used between distentions. The patient's position was then changed from sitting to supine or vice versa. The balloon probe was again positioned with the balloon at station 1 and the procedure was identically repeated. The proximal esophagus was distended first in both the sitting and supine positions to minimize the possibility that fatigue may UES " ~ ~ 1 f l. \ \ \ 5 em ~ LEVEL --f-- 5em UES' BALLOON LEVEL J : - '!. : ~ 1) J S T A T O N 5 em 5em FG. 1. Diagram showing the positions of the two esophageal transducer probes. Each probe had three strain gauge sensors, positioned 5 cm apart. One probe had its proximal sensor positioned in the upper esophageal sphincter (UES) and was not moved. The other probe had a balloon 2 cm above its most proximal sensor. A, the balloon probe is stationed with the balloon at the 3 and 4-cm level of the esophageal body (station 1). The balloon probe was repositioned in 2-cm increments during the experiment. B, the balloon probe is located with the balloon at the 15 and 16-cm level (station 7). This was the most distal distention site used. reduce the response rate of the proximal esophagus if the distal esophagus was first studied. Peristalsis was determined by measuring pressure peaks in each recording tip; a minimum of O.4-sec interval between recording tips (maximum speed of 12.5 cm per sec) classified a response as peristaltic. Pressure amplitude was determined by subtracting base line pressure from the measured value. A pressure rise of 20 mm Hg or greater occurring anywhere in the esophagus coincident with balloon distention was termed augmentation. f a secondary peristaltic wave was induced by distention, the distention site was considered the "site of elicitation" of that secondary peristaltic wave. The segment of the esophagus in which a secondary peristaltic wave was first recorded was termed its "site of origin." Statistical differences were evaluated by paired Student's t test. 9 Mean differences were calculated within subjects. The 5% level was used in determining the significance of the statistical tests. Results A total of356 intraluminal esophageal balloon distentions was analyzed in the 7 persons. Secondary peristalsis. No statistically significant difference existed in any result evaluated regarding secondary peristalsis between the supine and sitting positions. Therefore, all data are combined. Secondary peristaltic waves were propagated after 92 distentions. The site of origin within the esophagus could not be determined for five waves (subject 6) because the recording site proximal to the balloon malfunctioned. Results relating to secondary peristalsis are thus based on 87 waves. Of these, 86 waves originated in the esophageal body and 1 apparently originated in or above the UES. The recorded pressure complexes of secondary peristalsis always occurred after balloon deflation. The profile of the composite esophagus (7 subjects) demonstrated a progressive increase in secondary peristalsis incidence as the intraluminal distention site moved distally (fig. 2). No secondary peristalsis was elicited above the 7 and 8-cm level in the 6 subjects able to be tested above this level. The incidence of secondary peristalsis in the distal esophageal level tested (15 and 16-cm) was significantly greater than that recorded in the proximal 3 and 4-cm esophageal level (P < 0.01) and in the middle 9 and lo-cm esophageal level (p < 0.05). The mean incidence of secondary peristalsis was 60% at the 15 and 16-cm level. The incidence of secondary peristalsis in response to intraluminal distention was significantly less (P < 0.01) than the incidence of UES and proximal esophageal body augmentations (see below). To determine the origin of the secondary peristaltic wave, the esophagus was divided into a UES, a 0- to 5- cm segment, a 5- to 10-cm segment, and a 10- to 17-cm segment as required by the recording tip placement (fig. 1B). The origin of secondary peristalsis was placed in that segment which demonstrated the first pressure wave of a progressive complex at its distal site, i.e., it was placed in the 5- to 10-cm segment if the first pressure wave of a peristaltic wave occurred at the 10-cm recording site. As shown in table 1, the origin of 66

3 1294 ENZMANN ET AL. Vol. 72, No.6 80,..---,---, ,.--,---,...--, em LEV EL N ESOPH AGUS FG. 2. Mean incidence of secondary peristalsis in 7 subjects as a function of the distention site. The incidence of secondary peristalsis increased as the distention site moved distally and reached 60% when the balloon was inflated at the 15 and 16-cm level of the esophageal body. No statistical difference was present between the incidence recorded in the supine and sitting positions. STE OF ORGN UES 0-5 em 5-10 em em TOTAL a The site of origin of each of 87 secondary peristaltic waves recorded from 7 volunteers shown as a function of the site of esophageal balloon distention. One originated in or above the upper esophageal sphincter (UES); the remaining 86 originated within the esophageal body. Fifty-nine of the 86 secondary peristaltic waves originated in the esophageal body proximal to the distention site (stippled squares). The remaining 27 secondary peristaltic waves (type C) which originated in the esophageal body were first detected either at or below the site of intraluminal esophageal balloon distention. A total of 43 of the 86 (50%) secondary peristaltic waves originating within the esophageal body occurred at least 3 to 5 cm above the balloon distention site (stippled squares numbered 3, 24, and 16). secondary peristaltic waves occurred in the 5- to 10-cm esophageal segment (76%), 5 originated in the 0- to 5-cm segment (6%), and 15 originated in the 10- to 17-cm segment (17%). One (1%) secondary peristaltic wave apparently originated in or above the UES without associated UES relaxation. nasmuch as the experimental design always had a recording site within at least 5 cm proximal and 2 cm distal to the center of the balloon, the origin of secondary peristalsis in relationship to the balloon was characterized by three patterns of response as diagrammed in figure 3. Type A and B responses occurred when secondary peristalsis originated in the esophageal segment above the balloon (fig. 3). Type A differed from type B in that proximal esophageal body augmentation accompanied distention in type A responses (figs. 3, 4, and 58) whereas no augmentation occurred in type B (fig. 3). Type C responses were defined as those responses in which manometric evidence of secondary peristalsis was detected only at or below the balloon (figs. 3 and 5A). Esophageal body augmentation was a variable finding in type C responses. n all type C responses recorded, however, secondary peristalsis originated in the same esophageal segment as that in which balloon distention occurred (table 1). Thus, with this experimental design, the origin of type C secondary peristaltic waves could not definitely be shown to originate above the balloon, although such occurrence could not be excluded. Of the 86 secondary peristaltic waves originating in the esophageal body, 36 were type A, 23 type B, and 27 type C. The sites of origin of these secondary peristaltic waves as a function of the site of esophageal distention are demonstrated in table 1. This demonstrates that type A and type B responses, which comprise 59 of the 86 secondary peristaltic waves (69%), originated above the site of distention; 43 of the 59 type A and B responses originated a significant distance (at least 3 to 5 cm) above the site of balloon distention. The 27 type C responses represent those that could not be definitely determined to originate above the balloon. Type C responses occurred with increasing frequency when the closest cephalad recording site of the nonballoon probe was furthest from the balloon. This permitted a greater distance above the balloon in which a secondary peristaltic wave could originate without being detected by the recording site above the balloon. However, when the distention site was close to the first cephalad recording site of the nonballoon probe, such as station 5 (11 and 12 cm), the origin of 14 of 15 secondary peristaltic waves was recorded at this recording site (10-cm level of nonballoon probe) thus localizing the origin within the segment above the balloon. The one exception had a response of insufficient magnitude to be classified as a wave in the peristaltic complex. Although type C responses were recorded within this experimental design as occurring at or below the balloon, the above factors do not preclude their having originated above the balloon. - - TYPE A TYPE B P RXO ~ A ----W\.-- L STE TYPE C - --rl ~ ~ ~ BALLOON., ~ ~ 1st DSJAL l i f\ : :.1'1! i/\ S T '---~-H' ~ ~ '--- : : : : 2nd DSTAL!! /\ : : f\!! /\ S T'-- E ~ ~ '-- --t--y ~., : 3,d DSTAL: :./\. l./\. ~ ~ T E~ ~ ~ ~ FG. 3. Diagrammatic representation of the three types of esophageal secondary peristaltic response to intraluminal balloon distention. A pressure increase of 20 mm Hg or greater occurring in the esophageal body proximal to the distending balloon during balloon distention defined augmentation. Both type A and B responses were characterized by a secondary peristaltic wave whose origin within the esophageal body was recorded above the site of balloon distention. Type A responses differed from type B responses in that esophageal body augmentation occurred with type A responses. Type C responses were defined by the secondary peristaltic wave being detected at or below the site of balloon distention. Esophageal body augmentation was a variable finding in type C responses.

4 June 1977 ESOPHAGEAL RESPONSES TO NTRALUMNAL DSTENTON 1295 BD BD - - primary peristalsis was greater than the UES augmentation associated with balloon distention. 2 sec H '"""'. ~ : PNEUMOGRAPH : : f---_ !-! r-t-- A drop in UES resting pressure during distention f,, occurred 13 times (subjects 1, 2, and 7) accounting for C l 1 6, 0 ~ " less than 4% ofues responses (fig. 5B). The mean UES ~ ~ 80 : --ti-- pressure drop was 42 mm Hg and never fell below a ::e a : : --,,--:,--- recorded pressure of 10 mm Hg. The pressure drop lasted for the duration of distention except in four in -where it -lasted less than the distention dura H : ~ ~ Lstances E C 8 0 ~! tion. (,jj: i ~ ~ 4 ~ ~ Proximal ~ esophageal body. Position of the nonballoon BALLOON LEVEL, em BALLOON LEVEL, 80 VOl: 7ee lj 14cm f 40f _:: 13 em VOL,'.:: r4 ~ ~ ~, c em < 5 E 0-- i '18cm' '.: 'ZO cm ~ 40 ' ~ 8 0 ~ : E 0 _ "- - - ~ - -,,! ~ 4 8t 0 ~ = b f = = ~ :(G.l:sTRC), (GASTRC) ; ± ' = = = ' 5 = m ' = m ~ = _ ~ ~, b : 'A - - ~ FG. 4. Tracings of esophageal pressure records. DS, dry swallow; BD, duration of balloon distention; VOL, volume of the distended balloon. A, the frst sequence demonstrates a normal primary peristaltic wave initiated by a dry swallow. The three upper tracings were obtained from the three sensors of the nonballoon probe which recorded from the upper esophageal sphincter (UES) and the 5- and 10-cm levels of the esophageal body. The balloon was at the 11 and 12-cm level of the esophageal body. The lower three tracings were obtained from the balloon probe sensors which recorded from the 13- and 1S-cm levels of the esophageal body and the stomach. The second sequence shows the response resulting from balloon distention in the same subject. During distention, augmentation occurred above-the balloon and was recorded at the UES and 5- and 10-cm sensors. The secondary peristaltic wave which occurred after balloon deflation originated above the balloon and was frst recorded at the 10-cm level sensor; the wave was also recorded below the balloon at the 13- and 1S-cm levels of the esophageal body. This represents a type A secondary peristaltic response. B, balloon distention at the 13 and 14-cm level in another subject. Esophageal body augmentation occurred during distention but UES augmentation did not occur. The secondary peristaltic wave (type A) which occurred after balloon deflation was frst recorded at the 10-cm sensor which was 3 cm proximal to the balloon. UES. UES resting pressure measured 35 to 90 mm Hg for all subjects. A 20-mm Hg or greater pressure rise in UES resting pressure coincident with distention defined augmentation. The characteristic UES response to intraluminal esophageal body distention was augmentation (figs. 4A and 5A). Augmentation began with distention and ended with deflation with few exceptions in which the augmentation duration was less than distention duration. Augmentation was never maintained beyond deflation. The incidence of augmentation in subjects varied from 6% in subject 4 to 91 % in subject 1 (fig. 6). The low incidence in subject 4 is unexplained. The mean incidence of augmentation for all subjects was 63%. No statistically significant difference in the incidence of UES augmentation was found as a function of either the distention site or body position. The mean UES augmentation was 116 ± 38 SD mm Hg; neither body position nor the site of esophageal distention had a significant effect on this magnitude. For each subject the UES pressure rise occurring with recording tips permitted responses to be recorded only at the 5- and lo-cm levels of the esophageal body (fig. 1). This precluded ascertaining the precise proximal-most extent of the esophageal body response above the 5-cm level. Because of the experimental design, the proximal esophageal body (0- to 5-cm segment) response could only be studied when balloon distention occurred at or below the 7 and 8-cm segment. Esophageal responses at the 5- and 10-cm levels could be compared only when distention occurred below the 10-cm level. The esophagus proximal to the balloon and below the 2 sec P >-< : : PNEUMOGRAPH :: DS ~,, i ~ ~ ~ " ' ~ w '.:! o. => E H : ~ L J A Jl= L o 80 BAllOON LEVEl: 9 10 em E ~ f '. VOL: 6 cc ~ ~ 4 ~ t ~ _:,$ J\A.,, BALLOON LEVEL, em ~ 8 0 ~ ' : VOl:8cc ~ : ~ 40 :: 11 em! i 15 em EO, ~ 8 0 ~ ; ~ : : :r 40 i 16 em ; : A 20 em A ~ o ",,--- ~ ~ ~...! i f ~ 48000t ", 21 em, 25 em ~ f \ " ( G A S T R C ~ A '8. FG. 5. Tracings of esophageal pressure records. BD, duration of balloon distention; VOL, volume of the distended balloon; DS, dry swallow. A, the balloon was at the 9 and 10-cm level. A secondary peristaltic wave occurred after balloon deflation and was frst recorded at the 10-cm level sensor of the nonballoon probe. The wave then traversed the three sensors of the balloon probe which were at the 11-, 16-, and 21-cm levels of the esophageal body. This represents a type C secondary peristaltic wave. Augmentation occurred in the upper esophageal sphincter (UES) and 5-cm esophageal body sensors during balloon distention. B, responses to balloon distention and a dry swallow in another subject. After balloon deflation a secondary peristaltic wave (type A) was first recorded at the 10-cm level of the esophageal body which was 3 cm proximal to the balloon distention site. The peristaltic wave was also recorded below the balloon at the 15- and 20-cm levels of the esophageal body. Esophageal body augmentation occurred at the 5- and 10-cm level but the UES resting pressure dropped during balloon distention. The subsequent dry swallow showed a characteristic UES relaxation in contrast to the pressure drop recorded in the UES during balloon distention.

5 1296 ENZMANN ET AL. Vol. 72, No ,. - SUPNE - - STTNG _ - J!. ~ SUBJECT NUMBER FG. 6. The incidence of upper esophageal sphincter (UES) augmentation occurring during balloon distention in each of 7 volunteers. No statistically significant difference relating to position was found. UES responded to distention with augmentation over a segment of variable length (figs. 4 and 5). With few exceptions, esophageal body augmentation began with distention and ended with deflation. Exceptions were augmentation durations shorter than distention durations. nfrequently, a pressure rise occurred at one or more tips below the distending balloon but the presence or absence of this pressure rise had no relationship to the presence, onset, or m a g n iof t ~ u h~ e esophageal augmentation magnitude and the site of distention. Discussion This investigation was designed to d e t e r mt ~ i e ~ e site(s) of elicitation and origin of secondary penstalss in the human esophagus, characterize the U ~ a?d S proximal esophageal body r e s p o n s ~ s traluminal distention, and determme the relatonshp of these responses to secondary p e r i s t ~ l.. s i s.. This study demonstrates that the Ste of ~ h c 1 ; ~ t O n, site of origin, and incidence of secondary penstalss are a function of the distention site within the human esophagus. Because of the geometric arrangement of the two manometric probes, our study was confined to t ~ e a c c o m p a~ n ~ n g upper two-thirds of the esophagus. No s e c o n penstalsis was elicited after distention in the proxmal 6 c ~ ~ a r y of the esophageal body. Elicitation?f sec?ndary penstalsis below the 6-cm level progressvely mcreased as the distention site moved distally (fig. 2). The reason secondary peristalsis is not elicited in the proximal human esophagus is u n k n n o ~.man.' n. the upper 6 cm of the esophagus is compnsed pnm.anly.of striated muscle. lo n the monkey secondary perstalss, a u ~ e n. t a t i o n recorded proximal to the distenton Ste. The as determined by electrical p o t e n t i a ~ s, m C d ~ n c e of augmentation at the 5-cm level for the combmed only in smooth muscle when r e c o r were. d ~ obtamed g s supine and sitting position for each subject varied from from the transitional muscle zone whch contamed both 62 to 100%. The mean for all subjects was 85% ± 24 SD. A striated and smooth muscle. ll Secondary peristalsis, trend suggesting a higher incidence in the supine however has been elicited from striated muscle in the ~ o s ~ is d e m o n s t r ~ t e tion was not statistically significant (fig. 7). No statstcally significant difference in the incidence of doga and' cat.l2 The inability to elicit seco.ndary peristalsis in the proximal human esophagus S p r o b related to differences in striated and smooth muscle mner a ~ l y a u ~ e n tation at the 5-cm level was found as a functon of distention site. Again, a trend suggesting a higher incidence in the supine position was noted. The incidence of vation, although a myogenic basis for these differences cannot be excluded. augmentation at the 5-cm esophageal level.in!"esponse When a secondary peristaltic wave resulted from intraluminal esophageal balloon distention, it occurred to balloon distention was greater than the mcdence of UES augmentation (figs. 6 and 7). Although the 5-cm after balloon deflation and its site of origin was usually esophageal level and UES augmentation resp?nse often within the esophageal body proximal to the d i s t e n t i o ~ occurred simultaneously, either could occur wthout the site. The previous reported concept that secondary p e ~ other. stalsis usually originates at the UES2 was not substantated in this investigation. The site of origin of secondary Of all augmentations detected with the balloon located distally (13 and 14-cm and 15 and 16-cm levels), peristalsis was 1 to 5 cm proximal to the distention site the incidence was 32% at the 5-cm esophageal level only, 7% at the 10-cm level only (closer to the balloon), and 100 SUPNE 61 % in both locations simultaneously. These incidences - - STTNG represent combined upright and supine responses as no z 80 o significant positional difference occurred. These data i= «indicate the most frequent esophageal body response to ~ 60 w :;; balloon distention in the midesophagus is pressure augmentation involving a long segment (5- and 10-cm lev CJ ~ 40 els) proximal to the balloon. They also indicate that " 0 when augmentation occurs at only the 5- or 10-cm level, the incidence of response is significantly greater at the cm level than the lo-cm level, which is closer to the SUBJECT NUMBER balloon (P < 0.01). The magnitude of augmentation at the 5-cm level (mean, 49 mm Hg) and 10-cm level (mean, 40 mm Hg) did not differ significantly. Augmentation at both levels was of less magnitude than UES augmentation (P < 0.01). No relationship existed between the proximal FG. 7. The incidence of proximal esophageal body augmentation occurring during balloon distention at the 5-cm level in the supine and sitting positions for each of the 7 volunteers. No statistically significant difference was found between the sitting and supine positions although a trend toward a higher incidence in the supine position was present.

6 June 1977 ESOPHAGEAL RESPONSES TO NTRALUMNAL DSTENTON 1297 in 59 of the 86 (69%) secondary peristaltic waves which originated within the esophageal body; 43 of the 59 occurred at least 3 to 5 cm above the balloon distention site (50% of the total 86 secondary peristaltic waves elicited). The site of origin of the remaining secondary peristaltic waves may also have originated in the esophageal body proximal to the distention site, but experimental design precluded determining their precise site of origin. Our findings that the site of origin usually occurred in the esophageal body above the distending balloon contradicts most reports; previous investigators have localized the site of origin either at or below the site of esophageal distention4-8 or in or above the UES.2 Only Janssens et al., 3 in their investigation on dogs, have previously reported that secondary peristalsis usually started in the esophageal body above the site of stimulation. Although the reason for the contradiction between our findings and those of previous reports in man is unclear, it may be related to differences in the recording accuracy of the various manometric assembly systems used. The strain gauge esophageal probes used in our investigation have been demonstrated to be a suitable system for high fidelity recording of esophageal pressures. 13 t is reasonable to assume that noninfused catheter systems formerly used in human studies did not permit recognition that secondary peristalsis originated within the esophageal body above the distention site because the secondary peristaltic wave proximal to the balloon could not be separated from the augmentation response. With one exception (the secondary peristaltic wave which apparently originated in or above the UES), the origin of secondary peristalsis was never recorded more than 5 cm proximal to the distention site. The origin of secondary peristalsis was localized high in the esophageal body (0- to 5-cm segment) only with distentions occurring at the 7 and 8-cm and 9 and 10-cm levels (table 1); secondary peristaltic waves which originated lower in the esophagus occurred when the distention sites were also lower. The site of origin of secondary peristalsis within the esophageal body apparently moved distally as the esophageal distention site moved distally. Seventy-six per cent of elicited secondary peristaltic waves originated in the 5- to 10-cm esophageal segment. This percentage probably reflected experimental design artifact; distentions between 7 and 16 cm resulted in most secondary peristaltic waves originating in the 5- to 10-cm segment because the site of origin was usually 1 to 5 cm proximal to the distention site. The number of secondary peristaltic waves originating within the 10- to 17 -cm segment may have increased if distentions had been done at esophageal levels below 16 cm. The high percentage of secondary peristaltic waves which originated within the 5- to lo-cm esophageal body segment may, however, represent a greater reactivity of this segment. Reports on the UES response accompanying intraluminal esophageal body distention are contradictory Some authors report UES relaxation,2 others augmentation. 4 n contradistinction to the report of Siegel and Hendrix 2 that UES relaxation usually accompanied esophageal distention, we found UES pressure augmentation to be the characteristic response. Whereas they reported a 72% incidence ofues relaxation, we recorded a drop in UES resting pressure during less than 4% of distentions and an augmentation incidence of 63%. This difference in findings is unexplained. Our results are in accord with those of Creamer and Schlege1 4 who reported an 80% incidence ofues augmentation accompanying esophageal body balloon distention. No significant difference in the incidence of UES augmentation occurred with distentions throughout the proximal twothirds of the esophagus although a trend to decreasing response rate occurred as the balloon moved distally. Body position played no role in UES response. Repetitive UES augmentations have also been reported. 4 We did not find this response which may be explained by our shorter distention duration (3 to 5 sec versus 10 to 20 sec 4 ). The UES response was characterized by augmentation which occurred during balloon distention. The augmentation was ofless magnitude than the UES contraction pressure generated during primary peristalsis. Several authors have noted esophageal body responses proximal to the distention site.4-8 The most common response detected manometrically4' 7. 8 begins with balloon distention and ends with deflation and is characterized by a pressure rise which has been termed "spasm,"8 and simultaneous or nonperistaltic contractions (often repetitive).4. 7 An electrical response, initiated by balloon inflation, termed the "on response" has also been described. 5 6 The frequency of this proximal response reportedly varies from 48 to 90%. -H). 8 The proximal extent of this response in vivo has not been previously investigated. n an in vitro study, however, it has been reported that approximately 70% are local and present only immediately proximal to the balloon. 6 Our study confirmed that the esophageal body response proximal to the site of intraluminal distention was characterized by a pressure rise (augmentation) which occurred during balloon distention. The mean incidence of esophageal body augmentation occurring proximal to the balloon and recorded from the strain gauge 5 cm below the UES was 85% ± 24 SD. Augmentation at the 5.0-cm level was independent of the esophageal distention site within the proximal two-thirds of the esophagus. Our study further demonstrated that proximal esophageal body augmentation characteristically involved a long esophageal segment proximal to the balloon. The length of proximal esophageal body augmentation varied with the distention site; the further distal the distention site was from the UES, the longer the segment involved. The mean incidence of the esophageal body augmentation occurring proximal to the 13 and 14-cm and 15 and 16-cm distention sites which were detected simultaneously by strain gauges at both the 5- and 10- cm levels was 61%. Thus, balloon distention at sites in the midesophagus characteristically resulted in augmentation over at least a 5-cm long segment above the distending balloon. The segment lengthened from the proximal esophagus (below the UES) distally as opposed

7 1298 ENZMANN ET AL. Vol. 72, No. 6 to lengthening retrograde from the distention site. This was substantiated by the significantly greater incidence of augmentation (32%) which occurred at the 5-cm level only as compared to the 7% augmentation incidence which occurred at the 10-cm level only (P < 0.01) with distention done at the 13 and 14-cm and 15 and 16-cm levels of the esophagus. The exact proximal extent of augmentation was not determined but presumably involved the esophagus to the lower border of the UES. No statistically significant difference was found between the incidence of augmentation in the supine and sitting positions (fig. 7). This may be related to the few subjects studied and because in 2 subjects the incidence was the same. However, a definite trend was apparent toward a higher incidence of augmentation in the supine position. Augmentation did not occur below the balloon. On occasion, a pressure rise less than 20 mm Hg occurred at one or more tips below the balloon during inflation, but this had no relationship to the presence or magnitude of the pressure rise recorded proximal to the distention site. An infrequent response in the esophageal body below a distending balloon has been reported previously4 6 but, as in our study, had no relationship to the events recorded proximal to the distention site. Although proximal esophageal body and UES augmentation may occur independently, they usually occurred simultaneously. The proximal esophageal augmentation response was independent of secondary peristalsis elicitation. Secondary peristalsis did not depend on esophageal body augmentation proximal to the balloon as evidenced by the type B secondary peristaltic response (fig. 3). The safeguards of esophageal physiology against pharyngeal reflux appear to be well integrated. Upon intraluminal distention of the upper two-thirds of the human esophagus, the proximal esophagus augments its pressure over long segments. This augmentation begins proximally and extends for a variable length distally; it may extend to the site of distention. The UES usually augments its pressure in association with esophageal body augmentation. f the intraluminal distention occurs below the 5 and 6-cm level of the esophageal body, a secondary peristaltic wave may originate within the esophageal body above the site of distention upon balloon deflation. The incidence of secondary peristalsis initiation increases as the intraluminal distention site moves distally down the esophageal body. Augmentation of the UES and proximal esophageal body in response to esophageal intraluminal distention and the resultant initiation of secondary peristalsis above the site of distention comprise a highly integrated pressure barrier to esophagopharyngeal reflux. REFERENCES 1. Enzmann DR, Harell GS, Zboralske FF: Upper esophageal responses to intraluminal distention in humans (abstrj. Clin Res 23:130A, Siegel C, Hendrix TR: Evidence for the central mediation of secondary peristalsis in the esophagus. Bull Johns Hopkins Hosp 108: , Janssens J, Valembois P, Hellemans J, et al: Studies on the necessity of a bolus for the progression of secondary peristalsis in the canine esophagus. Gastroenterology 67: , Creamer B, Schlegel J: Motor responses of the esophagus to distention. J Appl Physiol 10: , Christensen J, Lund GF: Esophageal responses to distention and electrical stimulation. J Clin nvest 48: , Christensen J: Patterns and origin of some esophageal responses to stretch and electrical stimulation. Gastroenterology 59: , Winship DH, Zboralske FF: The esophageal propulsive force: esophageal response to acute obstruction. J Clin nvest 46: , Fleshier B, Hendrix TR, Kramer P, et al: The characteristics and similarity of primary and secondary peristalsis in the esophagus. J Clin nvest 38: , Goldstein A: Biostatistics-An ntroductory Text. New York, Macmillan Co, Treacy WL, Baggenstoss AH, Slocumb CH, et al: Scleroderma of the esophagus: a correlation of histologic and physiologic findings. Ann ntern Med 59: , Hellemans J, Vantrappen G, Valembois P, et al: Electrical activity of striated and smooth muscle ofthe esophagus. Am J Dig Dis 13: , Dodds WJ, Stewart ET, McCarthy LJ, et al: Esophageal labeling with small tantalum wires: effects on motility and histology. nvest Radiol 6: , Stef JJ, Dodds WJ, Hogan WJ, et al: ntraluminal esophageal manometry: an analysis of variables affecting recording fidelity of peristaltic pressures. Gastroenterology 67: , 1974