Effect of gastrin on antroduodenal motility: role of
intraluminal acidity
M.
Verkijk,
H. A. J.
Gielkens,
C. B. H. W.
Lamers, and
A. A. M.
Masclee
Department of Gastroenterology and Hepatology, Leiden University
Medical Center, 2300 RC Leiden, The Netherlands
 |
ABSTRACT |
The effect of
gastrin on the migrating motility complex (MMC) was studied in seven
healthy subjects. It was hypothesized that a potential effect of
gastrin on the MMC may result from intraluminal acidification through
increased gastric acid secretion. Therefore, antroduodenal manometry
and intraluminal acidity were recorded simultaneously. The effect of
gastric acid inhibition, with and without administration of gastrin, on
antroduodenal motility and intraluminal acidity was also evaluated and
compared with saline infusion (control). Continuous infusion of
gastrin-17 (20 pmol · kg
1 · h
1)
increased intragastric and intraduodenal acidity and suppressed phase
II and phase III motor activity in both antrum and duodenum. Concomitant gastric acid inhibition with intravenous famotidine, as
demonstrated by intragastric neutralization of pH, completely antagonized the effect of gastrin on the MMC. In fact, famotidine infusion, both with and without administration of gastrin,
significantly shortened MMC cycle length. It is concluded that the
effect of gastrin on interdigestive antroduodenal motility results from increased intraluminal acidity.
antroduodenal manometry; gastrin-17; famotidine; migrating motility
complex
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INTRODUCTION |
FASTING GASTROINTESTINAL motility in humans and several
other mammalian species is characterized by a recurrent pattern of cyclic occurring motor activity referred to as the migrating motility complex (MMC) (42). The MMC can be divided into at least
three distinct phases. Phase I is characterized by motor quiescence; phase II consists of spontaneous irregular motor activity that is
followed by phase III, a short burst of rhythmic contractions. Phase
III originates either in the stomach or the small intestine and
migrates distally.
Feeding interrupts the MMC cycle, i.e., phase III motor activity, at
all gastrointestinal sites. The subsequent postprandial or "fed"
motor pattern is characterized by persistent, irregular contractile
motor activity resembling in appearance fasting phase II (24, 26).
During the postprandial state, small intestinal motor activity is
suggested to promote efficient digestion, absorption and propulsion of
ingested material (34).
The mechanisms responsible for the postprandial interruption of the MMC
are not fully understood. Sham feeding delays the reappearance of phase
III motor activity, suggesting that the postprandial disruption of MMC
cycling may occur by cephalic neural stimulation (22). After the
ingestion of a meal, several gut hormones are released into the
circulation, of which cholecystokinin (CCK) is known to suppress the
MMC (25, 31). However, the lack of loxiglumide, a specific CCK-receptor
antagonist, to prevent disruption of the MMC after ingestion of a meal
(31) indicates that additional factors apart from the endogenous
release of CCK are involved in the conversion of the fasted into the
fed motor pattern.
Some studies indicate that gastrin may be involved in the postprandial
interruption of the MMC (15, 28, 41), but other studies argue against
this suggestion (13, 14, 43). The aim of the present study was to
investigate the effect of gastrin infused to postprandial plasma levels
on interdigestive antroduodenal motility. Gastrin is a potent stimulus
for gastric acid secretion (18). A potential effect of gastrin on
gastrointestinal motility may be dependent on, or regulated through,
intraluminal acidification by increased gastric acid secretion.
Therefore, intraluminal acidity was recorded simultaneously. In
addition, the effect of gastrin infusion combined with gastric acid
inhibition and of gastric acid inhibition alone on antroduodenal
motility and intraluminal acidity was evaluated.
 |
MATERIALS AND METHODS |
Subjects.
Seven healthy volunteers (2 men, 5 women; mean age 26 yr, range
18-54 yr) participated in the study. None of the subjects reported
a history of gastrointestinal symptoms or surgery or was taking any
medication. All were screened for Helicobacter pylori and had a negative serological status for IgG
antibodies against H. pylori. (ELISA)
(38). Informed consent was obtained from each individual, and the study
protocol had been approved by the local ethical committee.
Experimental design.
The subjects were studied on four separate occasions with an interval
of at least 7 days. All experiments were performed in a randomized,
single-blind (subjects), and placebo-controlled fashion. After an
overnight fast the subjects were intubated transnasally with a combined
manometry-pH assembly and a separate intragastric pH probe as described
below. Two intravenous cannulas, one for blood sampling and the other
for infusion, were inserted into the antecubital veins of each arm. The
subjects were studied in a semireclining position. Immediately after
the cessation of the first spontaneous phase III of the MMC in the
proximal duodenum, defined as time
30
min, the following intravenous infusions were started:
saline (control, A), gastrin-17
(B), gastrin-17 combined with acute
acid inhibition by famotidine (Pepcidine, Merck Sharp & Dohme, Haarlem,
The Netherlands) (C), or famotidine
alone (D). Infusion of famotidine
(20-mg bolus, continuous infusion 3.75 mg/h) was started at
time
30 min and continued until
time 360 min (16). Gastrin infusion
(20 pmol · kg
1 · h
1)
was always started 30 min later (time 0 min) and continued for 360 min. Saline infusions were
used as placebos for the experiments during which infusion of gastrin,
famotidine, or both (control) was not applied. Blood samples for
measurement of plasma gastrin were obtained at time
30,
15,
0,
30,
60,
90,
120,
150,
180, 240, 300,
and 360 min. Antroduodenal motility
and intraluminal pH were continuously monitored for 390 min after the
start of intravenous infusion of saline or famotidine, i.e., for 390 min after the cessation of the first registered spontaneous phase III
of the MMC in the proximal duodenum.
Monitoring of antroduodenal manometry and intraluminal pH.
Antroduodenal motility was measured by means of perfusion manometry.
Intraluminal pressures were recorded with a multilumen water-perfused
polyvinyl catheter (outer diameter 5 mm) that incorporated six side
holes located 0, 10, 12.5, 15, 20, and 25 cm from the distal tip. The
catheter was positioned under fluoroscopic control so that the most
proximal side hole was in the antrum. The side hole 15 cm from the
distal tip was always located in the proximal duodenum ~5 cm distal
to the pylorus. To monitor intraduodenal acidity, a miniature glass pH
electrode (model LoT440, InMedical, Mettler-Toledo, Switzerland) was
fixed to the manometry catheter with the tip of the pH electrode
180° opposite from the side hole located 15 cm from the distal tip.
A second and separate pH probe was positioned in the gastric corpus, 10 cm below the diaphragm. The manometry catheter was perfused
continuously with gas-free distilled water by a low-compliance
pneumohydraulic capillary infusion system (Arndorfer Medical Systems,
Greendale, WI) at a rate of 0.6 ml/min. Resistance to infusion within
the system was detected by a series of external transducers (Medex,
Hilliard, OH). Pressure and pH profiles were recorded with a polygraph
recorder (PC Polygraph VIII, Synectics Medical, Stockholm, Sweden),
displayed on a monitor, and stored on a personal computer for later
analysis. Intraluminal pH was sampled and stored at a rate of one
reading per second. The pH electrodes were calibrated in buffers of pH 1.4, 3.0, 4.0, and 7.0 before and after each experiment. The electrode drift at the end of each test was always <0.1 pH unit. At the end of
each experiment the correct positions of the manometry-pH assembly and
intragastric pH probe were verified by fluoroscopy.
Analysis of manometry data.
Antroduodenal motility recordings were analyzed both visually and
automatically. The individual tracings were processed by specialized
software (Polygram, Synectics Medical) for adjusting baselines and
extracting respiratory artifacts. However, the computer program does
not recognize simultaneous pressure events as artifacts. Therefore,
remaining artifacts obviously caused by increases in intra-abdominal
pressure were identified visually and excluded from analysis. Antral
motor characteristics were analyzed using the pressure tracings
recorded from the side hole located in the distal antrum. Duodenal
motor characteristics were analyzed using the pressure tracings
recorded from the side hole in the proximal duodenum, 12.5 cm from the
distal tip of the manometry catheter and 2.5 cm distal to the pH
electrode, and from the most distal side hole (0 cm). Antral phase III
activity was defined as rhythmic contractile activity at maximum
frequency (2-3 contractions/min) for at least 2 min in temporal
relationship with duodenal phase III activity (24) and was identified
visually. Duodenal phases of the MMC were characterized visually
according to the following definitions: phase I, motor quiescence;
phase II, irregular contractile activity at a rate of >2
contractions/10 min; phase III: regular rhythmic contractile activity
at a frequency of 10-12 contractions/min lasting for at least 2 min. Phase III had to be propagated over at least two recording sites.
MMC cycle length was defined as the time between the end of a phase III
in the duodenum and the end of the next phase III. Phase III
reoccurrence time was defined as the time interval between the start of
intravenous infusion of famotidine or saline (time
30 min) and the reoccurrence of a phase III.
When no reoccurrence of phase III activity was observed during the
total recording period of 390 min, phase III reoccurrence time was
arbitrarily set at 390 min. The following duodenal phase III
characteristics were determined visually: origin (antrum or duodenum),
duration (in s), and propagation velocity (in cm/min). Phase III
propagation velocity was defined as the time occupied by the front of a
duodenal phase III to propagate over 12.5 cm to the most distal
recording site in the duodenum. The frequency and amplitude of
individual contractions were measured for both phase II and phase III
using the computer program. Only pressure waves with amplitude
10
mmHg and duration
1.5 s were considered true contractions.
Additionally, motility indexes of the antrum and the proximal duodenum
were calculated for the last 30 min of phase II preceding duodenal
phase III. Motility indexes were calculated as the area under the
contraction curves, i.e., the sum of the area
(mmHg · s) under all individual contractions over a
period of 30 min.
Analysis of intraluminal acidity.
Intragastric pH readings, from a total recording period of 390 min,
were divided into 10-min intervals. For each 10-min period, the log
mean H+ concentration was
computed. The log mean H+
concentration was defined as the arithmetic mean of the antilog of the
pH data converted back into pH units by taking the log of the mean
value (35). Intraduodenal pH readings were analyzed for the 360-min
recording period during infusion of saline (control) or gastrin. The
log mean H+ concentration was
computed for 3-min intervals from 15 min before to 15 min after the
onset of each phase III in the proximal duodenum. Additionally, the pH
frequency distribution over 360 min was plotted.
Assay of gastrin.
Blood samples were collected in EDTA-containing ice-chilled tubes. The
samples were centrifuged at 3,000 rpm for 10 min at 4°C. All
samples were assayed in the same run. Plasma gastrin concentrations
were measured by a sensitive and specific radioimmunoassay using a
rabbit antiserum with equal binding to sulfated and unsulfated forms of
circulating gastrin, as described previously (20).
Statistical analysis.
Results are expressed as means ± SE. Data on late phase II and
phase III characteristics were not available for three subjects during
gastrin infusion because of complete interruption of the MMC.
Therefore, these data were pooled per treatment arm and were analyzed
for statistical significance by unpaired ANOVA. When ANOVA indicated a
probability of <0.05 for the null hypothesis, Student-Newman-Keuls
analyses were performed to determine which values differed
significantly (P < 0.05).
Differences in onset of phase III (antrum or duodenum) were analyzed by
-square analysis of contingency tables with Bonferroni's correction
for multiple comparisons. The remaining data concerning antroduodenal
motility, intraluminal acidity, and plasma gastrin, over time or
between treatment arms, were analyzed for statistical significance by multiple analysis of variance (MANOVA). When MANOVA indicated a
probability of <0.05 for the null hypothesis, Student-Newman-Keuls analyses were performed to determine which values differed
significantly (P < 0.05).
 |
RESULTS |
Plasma gastrin levels.
Basal plasma gastrin levels were not significantly different between
the four experiments: 18 ± 3, 21 ± 3, 21 ± 3, and 20 ± 4 ng/l for experiments A-D,
respectively. No significant alterations in plasma gastrin levels were
observed during control (experiment A). Continuous infusion of gastrin
(experiment B) resulted in significant (P < 0.05) increases in
plasma gastrin levels (Fig. 1). During
infusion of gastrin, plasma gastrin levels at ~140 ng/l were
obtained, comparable to peak postprandial levels (32). Concomitant
infusion of famotidine together with gastrin
(experiment C) resulted in
significantly (P < 0.05) higher
levels of plasma gastrin. Infusion of famotidine alone
(experiment D) induced a significant
(P < 0.05) rise in plasma gastrin
levels over control, starting from time 90 min.

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Fig. 1.
Plasma gastrin levels (means ± SE) in 7 healthy subjects during
intravenous infusion of saline (control, ), gastrin-17 ( ),
gastrin-17 combined with acute acid inhibition by famotidine ( ), and
famotidine alone ( ). * P < 0.05 compared with control, P < 0.05 compared with gastrin infusion.
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Intragastric and intraduodenal acidity.
Basal intragastric acidity was not significantly different between the
four experiments: pH 1.7 ± 0.1, 1.4 ± 0.1, 1.6 ± 0.1, and
1.6 ± 0.1 for experiments
A-D, respectively. No significant alterations in
intragastric acidity were observed during control. Infusion of gastrin
significantly (P < 0.05) increased
intragastric acidity within 90 min compared with control (Fig.
2). Famotidine, either with or without
gastrin infusion, significantly (P < 0.05) reduced intragastric acidity within 30 min compared with control, and pH > 4 was reached within 50 min after the onset of famotidine infusion.

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Fig. 2.
Intragastric log mean H+
concentrations (pH; mean ± SE) in 7 healthy subjects during
intravenous infusion of saline (control, ), gastrin-17 ( ),
gastrin-17 combined with acute acid inhibition by famotidine ( ), and
famotidine alone ( ). * P < 0.05 compared with control.
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Fluctuations in intraduodenal pH mainly occurred during phase II of the
MMC (Fig. 3). Infusion of gastrin
significantly (P < 0.05) increased
intraduodenal acidity for phase II compared with control (Fig.
4). The onset of phase III motor activity
in the proximal duodenum was always associated with a significant (P < 0.05) decline in intraduodenal
acidity to pH > 7, even during gastrin infusion (Fig.
5). Intraduodenal pH remained >6 during the subsequent phase of motor quiescence (phase I), and fluctuations did not occur until phase II motor activity had again returned in the
proximal duodenum. During concomitant infusion of famotidine together
with gastrin and during infusion of famotidine alone, intraduodenal pH
was >6 for 96 ± 3 and 98 ± 1%, respectively, of the total
recording time of 360 min (data not shown).

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Fig. 3.
Typical intraduodenal pH profile during late phase II, phase III, and
phase I of migrating motility complex (MMC) recorded in a healthy
subject during intravenous infusion of saline (control).
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Fig. 4.
Cumulative frequency distribution of intraduodenal pH for phase II in 7 healthy subjects during intravenous infusion of saline (crosshatched
bars) and gastrin-17 (solid bars) for 360 min.
* P < 0.05 compared with
control.
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Fig. 5.
Intraduodenal log mean H+
concentrations (pH; mean ± SE) in 3-min intervals from 15 min
before to 15 min after onset (time 0 min) of phase III motor activity in proximal duodenum
in 7 healthy subjects during intravenous infusion of saline (control,
top) and gastrin-17
(bottom) for 360 min.
* P < 0.05 compared with peak
in intraduodenal pH ( ) observed in 2nd 3-min interval after onset of
phase III motor activity (arrows).
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Antroduodenal motility.
The time interval between the start of the manometry recording and the
onset of the first spontaneous phase III in the proximal duodenum did
not significantly differ among the four experiments: 117 ± 38, 88 ± 22, 91 ± 25, and 104 ± 26 min for
experiments A-D, respectively.
Individual manometry tracings are shown in Fig. 6. During the control experiment, the
cycling frequency of the MMC, over a total recording period of 390 min,
was 0.4 ± 0.1 h
1 with a
phase III reoccurrence time of 136 ± 18 min (Table
1).

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Fig. 6.
Individual manometry tracings locating occurrences of phase III of MMC
in 7 healthy subjects during intravenous infusion of saline (control),
gastrin-17, gastrin-17 combined with acute acid inhibition by
famotidine, and famotidine alone. Open bars, duodenal phase III of
antral onset; closed bars, duodenal phase III of duodenal onset.
Subjects are arranged in same order for each experiment.
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Infusion of gastrin completely interrupted the cycling pattern of the
MMC in three of the seven subjects and prolonged phase III reoccurrence
time over control in three other subjects. In one subject, phase III
reoccurrence time was shorter during infusion of gastrin (97 min)
compared with control (203 min). Overall, phase III reoccurrence time
(7 subjects) was significantly (P < 0.05) prolonged during gastrin infusion (271 ± 45 min) compared with control (136 ± 18 min). The number of occurrences of phase III
recorded for each subject, over a total recording period of 390 min,
was reduced during infusion of gastrin (1.7 ± 0.7), although not
significantly, compared with control (2.3 ± 0.4) (Table
1). Because infusion of gastrin disrupted the cycling pattern of the MMC, either by prolonging phase III reoccurrence time or by completely suppressing phase III motor activity, complete MMC cycle length for
this experiment could not be determined. With regard to the different
phases of the MMC, relatively, although not significantly, less time of
the 360-min manometry recording period was occupied by phase I and
phase III motor activity compared with control (Table
2). Occurrences of phase III during
infusion of gastrin were all of duodenal origin (Table
3). The other phase III characteristics were not significantly different from control. The suppression of
antral motor activity during gastrin infusion was further reflected by
a significantly (P < 0.05) reduced
motility index for the antrum compared with control (Table
4). Similarly, the motility index for the
proximal duodenum was significantly (P < 0.05) reduced during gastrin infusion. Reduction of antral and
duodenal motility indexes during gastrin infusion resulted mainly from
a significant (P < 0.05) decline in
contraction frequency compared with control (Table 4).
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Table 4.
Motility characteristics of antrum and proximal duodenum for last 30 min of phase II preceding duodenal phase III
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Concomitant infusion of famotidine completely antagonized the effect of
gastrin on the MMC (Tables 1-4). In fact, phase III reoccurrence
time tended to be shorter compared with control. The latter was
reflected by a significantly (P < 0.05) reduced individual mean MMC cycle length compared with control
(Table 1). This shorter duration of the MMC cycle resulted from a
significant (P < 0.05) reduction in
phase II duration compared with control. Furthermore, the relative
contribution of phase I (P = 0.14) and phase III (P < 0.05) motor activity
to the 360-min manometry recording period was increased over control
during concomitant infusion of famotidine together with gastrin. The
latter was further reflected by a significant
(P < 0.05) reduction in the
contribution of phase II motor activity (Table 2). Phase III
characteristics did not significantly differ from control (Table 3).
Likewise, antral and duodenal motility indexes for phase II were not
significantly different from control (Table 4). The effect of
concomitant infusion of famotidine together with gastrin on the MMC was
similar to that of infusion of famotidine alone (Tables 1-4).
 |
DISCUSSION |
The present study shows that exogenous gastrin infused to postprandial
plasma levels interrupts the cycling pattern of the MMC by suppressing
gastric onset of phase III motor activity and prolonging the
reoccurrence of phase III motor activity in the duodenum. Infusion of
gastrin reduced phase II motor activity in both the antrum and the
duodenum. Our findings indicate that the effect of gastrin on
gastrointestinal motility results from increased intraluminal acidity,
because it is no longer observed during gastrin infusion and
concomitant gastric acid inhibition with famotidine. Finally, we have
shown that inhibition of gastric acid secretion with famotidine has a
promoting effect on the occurrence of the MMC by shortening its cycle
length.
Our results are in agreement with those of Erckenbrecht et al. (15),
showing that infusion of pentagastrin without gastric acid inhibition
interrupts the interdigestive motor pattern. These authors concluded
that gastrin is a likely candidate for the postprandial interruption of
the MMC. Our results suggest that gastrin itself is probably not
involved in the postprandial interruption of the MMC, because gastric
acid inhibition with famotidine completely antagonized the effect of
gastrin on antroduodenal motility. Similarly, Dooley et al. (13) have
shown that gastrin-17 infused to postprandial plasma levels combined
with continuous gastric aspiration does not affect interdigestive
intestinal motility. In contrast to our study, however, the
interventions in the latter study were not timed with respect to the
different phases of the MMC cycle. Furthermore, only the number of
occurrences of intestinal phase III were included in their analysis on
MMC cycling, which therefore neglected the temporal organization of the
MMC. In the canine species, both pentagastrin and gastrin-17, with or
without continuous gastric aspiration, were reported to interrupt the
MMC (28, 41, 43). Despite these observations, the role of gastrin in the postprandial interruption of the MMC has been questioned in this
species because 1) certain food
substances that interrupt the MMC lack the ability to stimulate
endogenous gastrin release (14) and
2) infusion of pentagastrin fails to
interrupt the MMC in the distal small intestine (43).
Suppression of interdigestive gastrointestinal motility by gastric acid
was also demonstrated in patients with gastric acid hypersecretion. In
these patients, interdigestive gastrointestinal motility is
characterized by a reduced occurrence of both antral and duodenal phase
III compared with normosecretory subjects (8, 19). Pharmacological
inhibition of gastric acid secretion (6) and intragastric
neutralization of pH with sodium bicarbonate (9) restore the
interdigestive motor pattern in this group of patients to that seen in
healthy subjects. Similarly, stimulation of gastric acid secretion in
healthy subjects prolongs the cycling rate of the MMC (6, 8). Although
intraluminal acidification appears to be a potent inhibitor of
gastrointestinal motility, it might be questioned at this point whether
its effect on motility originates in the stomach or the duodenum.
Previous studies in the canine species suggest that the proximal
duodenum is a sensitive site for inhibition of gastric emptying through
intraluminal acidification (11, 30). In humans, Misiewicz et al. (33)
demonstrated that infusion of pentagastrin during continuous aspiration
of gastric contents did not inhibit gastric motility until gastric acid
was allowed to enter the duodenum. Likewise, Couturier et al. (12)
showed that intragastric acid infusion in humans inhibits gastric
myoelectrical activity to the same extent as intraduodenal infusion of
acid at infusion rates that resembled gastric emptying of the solution
studied during intragastric infusion. Therefore, the duodenum should be considered as a potential site through which gastrin exerts its effect
on antroduodenal motility by intraluminal acidification as in the
present study. Our study design, however, does not allow us to exclude
an effect of gastrin on motility resulting from intragastric
acidification.
Motilin may play an important role in the initiation of phase III in
the stomach. Motilin is released periodically during the interdigestive
state, and two- to threefold increments in plasma motilin are related
to occurrences of phase III that originate in the stomach (36).
Furthermore, infusion of motilin induces premature phase III motor
activity in the stomach (21) and anti-motilin serum in the canine
species suppresses the occurrence of spontaneous gastric phase III
(27). Woodtli and Owyang (44) showed that intraduodenal acid infusion
in humans suppresses antral motor activity without affecting the
cycling pattern of plasma motilin levels, suggesting that, at least in
humans, intraduodenal acidification may reduce the action of motilin on
the stomach. The intestinal motor response to intraduodenal acid
infusion may include postponement of phase III motor activity but,
occasionally, also induction of phase III-like complexes (29, 44).
Animal studies suggest the involvement of both vagovagal and intramural
neural pathways in the gastrointestinal motor response to intraluminal
acidification (1, 17, 45).
Apart from neural pathways mediating the effect of intraluminal
acidification on gastrointestinal motility, hormonal mechanisms should
not be ruled out. For instance, duodenal acidification is known to
release secretin (5) and could thereby influence gastric motility (37).
Furthermore, release of CCK (10) and motilin (5) has been reported
during intraduodenal acidification of which CCK is known to suppress
the MMC (25, 31). The role of motilin is probably limited as discussed
above.
The role of gastric acid as a potential modulator of interdigestive
gastrointestinal motility is further emphasized by our present data
demonstrating that gastric acid inhibition with famotidine significantly shortens MMC cycle length. In vitro studies have shown
that histamine H2-receptor
antagonists exhibit cholinergic-like effects (3, 4). In fact,
H2-receptor antagonists
dose-dependently inhibit acetylcholinesterase activity (2, 39). It
might therefore be questioned whether famotidine exerts its promoting
effect on the occurrence of the MMC through a direct interaction with
the cholinergic system rather than through inhibition of gastric acid secretion. Several studies, however, have shown that the cholinergic effect of H2-receptor antagonists
varies widely between different compounds (2, 4), that of famotidine
being the weakest (2). Furthermore, no inhibition of
acetylcholinesterase activity could be demonstrated in vivo when
therapeutic doses of H2-receptor antagonists were applied (40). Finally, our results are in accordance with those of Bortolotti et al. (7) who used the proton-pump inhibitor
omeprazole instead of a
H2-receptor antagonist to inhibit gastric acid secretion.
We have demonstrated, in agreement with previous studies (19, 44), that
intraluminal acidity of the proximal duodenum is closely related to the
different phases of the MMC. Fluctuations in intraduodenal pH mainly
occurred during phase II of the MMC. Onset of phase III motor activity
in the duodenum was always characterized by a rapid increase in
intraduodenal pH that remained in the neutral range during the
subsequent phase of motor quiescence. During the interdigestive state,
the MMC is accompanied by a true cycling secretory component involving
pancreatic, biliary, and gastric secretion (23). It has been suggested
by Woodtli and Owyang (44) that the cycling variation of intraduodenal
pH most likely results from these secretory processes. We have shown,
however, that the onset of duodenal phase III motor activity always
preceded the onset of intraduodenal neutralization of pH, even during
continuous stimulation of one of these secretory processes, i.e.,
gastric acid secretion. Although our study does not allow us to exclude an effect resulting from gastrointestinal secretion, the temporal sequence of these events suggests that duodenal phase III motor activity itself may be an important factor contributing to the increase
in intraduodenal pH around duodenal phase III.
It is concluded that in humans 1)
gastrin infused to postprandial plasma levels increases intraluminal
acidity and suppresses interdigestive antroduodenal motility;
2) the effect of gastrin on
antroduodenal motility results from increased intraluminal acidity;
3) inhibition of gastric acid
secretion significantly shortens MMC cycle length; and
4) gastrin itself seems not to be
involved in the postprandial interruption of the MMC.
 |
FOOTNOTES |
Address for reprint requests: A. A. M. Masclee, Dept. of
Gastroenterology-Hepatology, Leiden Univ. Medical Centre (LUMC), Bldg.
1, C4-P, PO Box 9600, 2300 RC Leiden, The Netherlands.
Received 11 September 1997; accepted in final form 29 June 1998.
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