Wim J. E. P. Lammers, Luc Ver Donck, Betty Stephen, Dirk Smets and Jan A. J.

Schuurkes
Am J Physiol Gastrointest Liver Physiol 296:1200-1210, 2009. First published Apr 9, 2009;
doi:10.1152/ajpgi.90581.2008
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Am J Physiol Gastrointest Liver Physiol 296: G1200G1210, 2009.

First published April 9, 2009; doi:10.1152/ajpgi.90581.2008.

Origin and propagation of the slow wave in the canine stomach: the outlines
of a gastric conduction system
Wim J. E. P. Lammers,1 Luc Ver Donck,2 Betty Stephen,1 Dirk Smets,2 and Jan A. J. Schuurkes3
1

Faculty of Medicine and Health Sciences, Department of Physiology, United Arab Emirates University, Al Ain, United Arab
Emirates; 2Department of Internal Medicine, Johnson & Johnson Pharmaceutical Research and Development, a Division
of Janssen Pharmaceutica, Beerse, Belgium; and 3Movetis, Turnhout, Belgium
Submitted 6 October 2008; accepted in final form 6 April 2009

Recently, systems that allow high-density recordings using

large numbers of extracellular electrodes have been introduced
to reconstruct in greater detail the origin and propagation of
electrical signals in the small intestine (22, 25, 27). A first
study describing origin and pathways of disrupted slow wave
propagation during gastric arrhythmias has been performed
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Lammers WJ, Ver Donck L, Stephen B, Smets D, Schuurkes

JA. Origin and propagation of the slow wave in the canine stomach:
the outlines of a gastric conduction system. Am J Physiol Gastrointest
Liver Physiol 296: G1200 G1210, 2009. First published April 9,
2009; doi:10.1152/ajpgi.90581.2008.Slow waves are known to
originate orally in the stomach and to propagate toward the antrum,
but the exact location of the pacemaker and the precise pattern of
propagation have not yet been studied. Using assemblies of 240
extracellular electrodes, simultaneous recordings of electrical activity
were made on the fundus, corpus, and antrum in open abdominal
anesthetized dogs. The signals were analyzed off-line, pathways of
slow wave propagation were reconstructed, and slow wave velocities
and amplitudes were measured. The gastric pacemaker is located in
the upper part of the fundus, along the greater curvature. Extracellularly recorded slow waves in the pacemaker area exhibited large
amplitudes (1.8 1.0 mV) and rapid velocities (1.5 0.9 cm/s),
whereas propagation in the remainder of the fundus and in the corpus
was slow (0.5 0.2 cm/s) with low-amplitude waveforms (0.8 0.5
mV). In the antrum, slow wave propagation was fast (1.5 0.6 cm/s)
with large amplitude deflections (2.0 1.3 mV). Two areas were
identified where slow waves did not propagate, the first in the oral
medial fundus and the second distal in the antrum. Finally, recordings
from the entire ventral surface revealed the presence of three to five
simultaneously propagating slow waves. High resolution mapping of
the origin and propagation of the slow wave in the canine stomach
revealed areas of high amplitude and rapid velocity, areas with
fractionated low amplitude and low velocity, and areas with no
propagation; all these components together constitute the elements of
a gastric conduction system.
slow wave; pacemaker; velocity; amplitude; gastric conduction system
THE FIRST ELECTRICAL RECORDINGS from the serosal gastric surface have shown the omnipresence of the slow wave cycle (1,
5, 30, 46). Kelly and coworkers (18, 19) used 6 10 extracellular electrodes sutured to the stomach to determine the origin
and the pattern of propagation of the gastric slow wave. Similar
studies were performed with electrodes oriented in the longitudinal direction along the greater curvature, midway between
the greater and the lesser curvature, and oriented in the circular
direction (7, 20, 34, 35). All of these studies have expanded on
the original concept of a slow wave that seemingly originates
from the mid- or the upper corpus, does not activate the fundus,
and propagates aborally with gradually increasing velocity and
amplitude (42).

Address for reprint requests and other correspondence: W. J. E. P. Lammers,

Dept. of Physiology, Faculty of Medicine and Health Sciences, P.O.Box
17666, Al Ain, United Arab Emirates (e-mail: wlammers@smoothmap.org).
G1200

Fig. 1. Recording electrode arrays used in this study and their locations on the
ventral surface of the canine stomach. A: two types of electrode arrays were
used to record slow wave activity at high resolution from particular areas: a
rectangular electrode was used on the corpus (location C) and an octagonal
array that was positioned on either the fundus or oral corpus (F1, F2), on the
corpus/antrum (location C-A), or the antro-duodenal area (location A-D).
B: size and electrode distribution of the large electrode array shaped to cover
as much as possible the ventral stomach surface. Interelectrode distances:
rectangular array: 2 mm; octagonal array: 2.5 mm; large array; 5 mm. These
panels are shown as insets in Figs. 2 6 to indicate the position of the electrode
array on the stomach.

0193-1857/09 $8.00 Copyright 2009 the American Physiological Society

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ORIGIN AND PROPAGATION OF GASTRIC SLOW WAVES

with a similar recording technique (28). In the current study,

several electrode arrays were used to perform detailed reconstruction of the normal propagation of the slow wave in several
areas of the canine stomach ranging from the oral fundus to the
distal antrum.
METHODS

Eighteen overnight fasted dogs (beagles, 10.9 2.1 kg; 14 females, 4 males) were used in this study. Anesthesia was induced with
scopolamine (0.015 mg/kg), lofentanil (0.070 mg/kg), and succinylcholine (1 mg/kg) and maintained throughout the duration of the
experiments (3 4 h) with etomidate (1.5 mg kg1 h1) and fentanyl
(0.025 mg kg1 h1). The animals were ventilated through a tracheal
tube, and the left femoral artery was cannulated to record systemic
blood pressure. Vital signs such as heart rate and blood pressure were
monitored continuously as previously described (25). Housing, care,

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type of anesthesia, and experimental procedures were approved by the

institutional ethics committee.
Following a median laparotomy, the abdominal walls were slightly
retracted, and one of three available electrode arrays was carefully
positioned on the ventral surface of the stomach. The electrode tips
were flush with the recording surface of the assembly, and there were
no protruding sharp edges that might otherwise have adversely affected the underlying tissue. A probe to monitor temperature in the
experimental area was positioned alongside the stomach, and a heat
lamp maintained the area at body temperature. After positioning the
electrode assembly, the stomach was allowed to stabilize for 10 min
before recordings were performed. At the end of the experiment, the
animals were killed (pentobarbital sodium, 200 mg/kg iv).
Three different electrode arrays (Fig. 1), each containing 240
recording electrodes, were used: 1) a rectangular array (46 18 mm;
interelectrode distance 2.0 mm), 2) an octagonal array (40 38 mm;
interelectrode distance 2.5 mm), and 3) a large, slightly curved, array

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Fig. 2. A: location of the rectangular electrode array on the canine corpus (C in Fig. 1). B: 24 electrograms recorded in the longitudinal direction. The red bars
indicate the local timings of the first slow wave (in s) at each electrode location and, in the second slow wave, the blue brackets plot the amplitude of the
waveforms. C: activation times for each individual electrode [time (t) 0 ms at the electrode in top left]. Isochrones were drawn manually around areas activated
in steps of 1 s. The drawing of the grid was expanded horizontally to accommodate the digits. The column with circled digits represents the electrodes
corresponding to the electrograms shown in B. D: slow wave propagation map in which the individual activation times have been left out and replaced by colored
isochrones with additional symbols indicating timing (in s) and direction of propagation. The row with white circles indicates the electrogram recordings shown
in B. E: display of direction and magnitude of local conduction velocities. F: mean velocity and amplitude (SD) as calculated from values averaged along rows
(indicated by the dashed rectangles in E) perpendicular to the red dotted line. Note that the no. of velocity bars is one less than the amplitude bars as the velocities
are calculated across neighboring electrode sites (25), whereas amplitudes are measured at each site.
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Table 1. Conduction velocity, amplitude, and frequency

in four gastric regions
Pacemaker Area

Velocity, cm/s*
Amplitude, mV*
Frequency, cycle/min
No. of maps/dogs

1.520.91
1.761.04
5.40.9
7/5

Fundus

Corpus

Antrum

0.390.21 0.490.14 1.480.57

0.690.44 0.900.52 2.021.27
4.90.7
5.20.4
5.00.7
5/4
6/6
14/14

All values are means SD. *P 0.001 (ANOVA). P 0.05, pacemaker

area or antrum compared with fundus or corpus (Tukey).

Fig. 3. Initiation of the slow wave along the

greater curvature close to the gastro-esophageal
junction (F1 in Fig. 1). A: 16 signals recorded
along the path of the slow wave (locations
shown in white circles in B). Electrograms 19
display high-amplitude bi- or triphasic waveforms, whereas electrograms 10 16 show lowamplitude fractionated waveforms. B: propagation map of the slow wave with initial rapid
propagation in the first 2 s (indicated by
wider-spaced isochrones) and slower propagation thereafter (crowding of the isochrones). Isochrones are drawn every 0.5 s. The
left side of the map, distant from the greater
curvature, is not excited at all (block symbol;
gray zone). C: local directions of conduction
and velocity. The velocities were averaged in
rows along the red dotted line and plotted in D
demonstrating velocities of 1.5 cm/s in the
area activated in the initial 2 s of propagation
and velocities of 0.5 cm/s beyond this area. A
similar pattern was seen with the slow wave
amplitude.

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(100 80 mm; interelectrode distance 5.0 mm). The rectangular array

was used on the corpus (location C), whereas the octagonal array was
used on the fundus, the oral corpus (locations F1 or F2), the antrum
(location C-A), or on the pyloric region (location A-D). The large
array (Fig. 1B) was positioned to cover the entire ventral surface of the
stomach. Unipolar electrical recordings were performed with a subcutaneous needle in the back right leg acting as the indifferent pole.
The 240 recording electrodes were connected through shielded wires
to 240 AC preamplifiers where the signals were amplified (4,000),
filtered (2 400 Hz), and digitized (1-kHz sampling rate) before being
stored on the hard disk of a laptop.
For the off-line analysis, signals were digitally filtered (20-point
moving average; low pass filter of 40 Hz) and displayed on screen
in sets of 10 30 electrograms (Fig. 2B). The activation time of a slow
wave was determined as the point of maximal negative slope (25) and

was marked with a cursor. The peak-to-peak amplitude of each

waveform was also measured (Fig. 2B, inset). The activation times of
each wave were then displayed on a grid representing the layout of the
original recording electrode array (Fig. 2C). All activation times were
related to the timing of the first slow wave detected in a map
[electrode on top left; time (t) 0.0 s]. Isochrones were drawn
manually around areas activated in steps of 1 s (Fig. 2, C and D). From
the local activation times, the direction and the magnitude of the slow
wave propagation was calculated and plotted (Fig. 2E) (25). These
velocities were then averaged in the direction of propagation (red
dashed line) and plotted in a bar chart (Fig. 2F). The amplitudes of the
local waveforms were also averaged in the direction of propagation
and plotted in a similar manner.
A total of 57 recordings were made, ranging in duration from 2 to
6 min (average recording duration 4.7 min, total recorded time 270
min). After the experiment, all electrograms in a 64-s period were
analyzed, and maps were created to determine the quality of the
recordings and the major pattern of slow wave propagation. Once the
pattern of propagation in a particular recording had been determined,
a representative set of 10 24 electrograms was visually inspected
while playing back the signals for the duration of the whole recording.
If changes in rhythm or in sequence of excitation occurred, additional
detailed analysis of such events was performed on all 240 electrograms. In this study, a total of 63 periods (67 min) was analyzed at this
high resolution. The frequency of the normal rhythm was determined
by measuring the cycle-to-cycle length of each successive slow wave
in one representative electrogram.

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ORIGIN AND PROPAGATION OF GASTRIC SLOW WAVES

It is important to note that the extracellular recording technique

used in this study only records the extracellular current generated by
the depolarization of the slow wave potential and does not record the
plateau nor the repolarization phase of the slow wave (4, 5, 17).
Furthermore, because the dimension of the electrode tip (0.3 mm
diameter) is quite large compared with the size of the cells, the
potentials recorded are the sum of the depolarization of hundreds of
cells in the recorded region.
Data are presented as means and SDs. Where appropriate, ANOVA
was used to evaluate differences for statistical significance.
RESULTS

Fig. 4. Spontaneous variations in spatial spread

of propagation in the oral fundic area (F1 in Fig.
1). Top: 16 electrograms from the canine fundus
(locations shown in circles in A and B). Bottom:
propagation maps A and B corresponding to the
slow wave cycles A and B in top. Slow waves
were initiated midway of the right border
along the greater curvature and propagated
predominantly aborally. Large areas of the
map were not excited (gray area). However,
the slow wave in map B propagated further in
the fundus than the one in map A. Similar
spontaneous variations in the distance of slow
wave propagation are visible in the previous
and subsequent slow wave cycles as shown in
the waveforms in the tracings on top.

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Figure 2 presents the major characteristics of slow wave

propagation in the canine corpus. The waveforms had a
relatively low amplitude (0.88 0.43 mV) and often
showed multiple small deflections similar to fractionated
electrograms in the heart (Fig. 2B, inset) (10). The pattern of
propagation in the corpus (Fig. 2D) was uniform, slightly curved
toward the lesser curvature, and had a constant propagation
velocity of 0.5 cm/s. Similar results were seen in five other dogs
(Table 1).
Figures 35 present the pattern of propagation of the slow
wave in the canine fundus. At the most oral location (F1 as
indicated in Fig. 1), slow wave propagation was limited to the

area adjacent to the greater curvature. Initial waveforms in that

area showed high amplitude (1 mV; Fig. 3A), and the
velocity map displayed rapid propagation of 1.6 cm/s (Fig. 3,
C and D). After the slow wave had propagated for 2 s,
velocity decreased to 0.5 cm/s and amplitude to 0.8 mV.
The oral part of the fundus is only partially exited by the
slow wave that originates from the greater curvature. In Fig.
3, the distance travelled by the slow wave from the greater
curvature in the fundus, before being blocked, was 20 mm.
This distance could vary from one slow wave to another, as
shown in Fig. 4. In that recording, spontaneous variations
occurred ranging from 10 to 22 mm (Fig. 4, slow waves A
and B). The width of this excited area was measured in five
dogs and varied between 15 and 30 mm (average 22 5
mm). In the distal fundus (location F2; Fig. 5), no areas of
inexcitability were detected (four dogs). The pattern of
propagation in the distal fundus was uniform, with low
amplitude signals (0.65 mV), fractionated waveforms (Fig.
5A), and a constant low velocity of 0.35 cm/s.
Unlike the pattern of propagation in the canine corpus, the
antrum showed high-amplitude signals (3.1 mV; Fig. 6A) and
high velocity (1.6 cm/s; Fig. 6D). Similar patterns and amplitudes were observed in 14 dogs (Table 1).

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ORIGIN AND PROPAGATION OF GASTRIC SLOW WAVES

The slow wave did not propagate across the pylorus but was
blocked at the antro-duodenal junction (Fig. 7). An area where
no propagation occurred was always found between the region
activated by the stomach pacemaker and the region activated
by the duodenal pacemaker. The length of this unexcited
region was 9.7 4.6 mm (n 5 dogs). Additionally, spikes
could be seen in most dogs at 511 locations in the distal
antrum (10% of the total area activated in the antrum). The
spike patch shown in Fig. 7C was one of the largest seen in this
study.
In four dogs, the large electrode array (Fig. 1B) was used to
record from the entire ventral surface of the stomach. As
shown in Fig. 8A, slow waves were regularly initiated at a
frequency of 5.5 cycle/min from a site located near the esophageal junction on the fundus (Fig. 8B). Propagation of the slow
wave occurred uniformly along the length of the stomach and
took 40 50 s to reach the distal stomach. Occasionally, a
slow wave was blocked that momentarily decreased the frequency in the distal stomach (Fig. 8A).

Because of the time required for the slow wave to reach the
distal antrum, new slow waves were already being generated
while previous slow waves were still propagating in the aboral
direction. As indicated by the vertical line in Fig. 8A, there
were four separate slow waves propagating simultaneously
along the stomach at that moment in time (Fig. 8C, waves a, b,
c, and d). In the accompanying animation,1 it can be seen that
the number of simultaneously propagating slow waves fluctuated between three and five.
The velocity and the amplitude of the slow wave, as it
propagated from the oral fundus to the distal antrum, was
measured as shown in Figs. 2, 3, 5, and 6. This was done for
a total of 32 maps, recorded from locations F1, F2, C, and C-A
(Fig. 9). For the majority of the stomach, the amplitude and
velocity of the slow wave was constant at 0.9 mV and 0.5
1
An animation of slow wave propagation (Fig. 8) is available at www.
smoothmap.org or at www.youtube.com, search stomach slow wave propagations.

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Fig. 5. Pattern of slow wave propagation in the distal fundus (F2 in Fig. 1). A: electrograms 117 recorded in the direction of propagation (locations shown in
B). Slow waves showed low amplitude and fractionated waveforms. B: map of the slow wave demonstrating slow and uniform propagation. C: local conduction
velocities. The velocities and amplitudes were averaged along the red dashed line and plotted in D, illustrating a uniform and low velocity throughout this region
of 0.35 cm/s and a mean amplitude of 0.65 mV.

ORIGIN AND PROPAGATION OF GASTRIC SLOW WAVES

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cm/s, respectively. In the pacemaker area, located in the oral

fundus, and in the antrum, slow wave velocity was significantly
higher (1.52 0.91 and 1.48 0.57 cm/s, respectively; P
0.001, Table 1) as was the amplitude of the waveforms (1.76
1.04 and 2.02 1.27 cm/s, respectively; P 0.001; Table 1).
The frequency of the slow waves was similar in the different
regions of the stomach (P 0.832; Table 1).

DISCUSSION

The major findings in this first high-resolution electrical

mapping of the stomach are: 1) the slow wave pacemaker is
located along the greater curvature high in the fundic area,
2) the pacemaker area is characterized by high-amplitude
potentials (1.8 mV) and high-propagation velocity (1.5 cm/s),

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Fig. 6. Slow wave propagation in the canine corpus

and antrum (C-A in Fig. 1). A: 17 electrograms
recorded along the major direction of propagation.
In the corpus, slow wave propagation was constant
with low-amplitude fractionated deflections, while
at electrode 9, propagation velocity and slow wave
amplitude increased as the slow wave propagated in
the antrum. B: corresponding propagation map with
closely spaced isochrones in the corpus (indicating
slow velocity) and widely spaced isochrones in the
antrum (indicating rapid propagation). C: local direction and velocity of propagation measured in the
corpus and the antrum. The velocities and amplitudes were averaged along the direction of propagation (red dashed line) and plotted in D. Average
velocity in the corpus was 0.45 0.14 cm/s, which
increased to 1.52 1.05 cm/s in the antrum,
whereas the amplitude increased from 1.15 0.46
to 3.04 1.43 mV.

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ORIGIN AND PROPAGATION OF GASTRIC SLOW WAVES

3) propagation through the distal fundus and the corpus is slow

(0.4 0.5 cm/s) with fractionated low-amplitude (0.4 0.9 mV)
potentials, and 4) propagation in the antrum is fast (1.5 cm/s)
with high-amplitude potentials (2.0 mV). Finally, because of
the long distance between the pacemaker area and the distal
antrum, the overall low propagation velocity, and the frequency of the pacemaker, there are three to five separate slow
waves propagating simultaneously along the stomach.
Several of these findings constitute significant expansions of
earlier results. For example, the location of the pacemaker, as
determined by electrical recordings (18, 20) or surgical incisions (19, 46), has been assumed to be located along the greater
curvature. The results in this study support that concept but
suggest a more oral location. This refinement was made possible by the high spatial resolution of the recording electrodes
(2 mm interelectrode distance in 2 dimensions), which makes
it possible to identify the propagation of low-amplitude signals
from one location to the next (Fig. 2B, inset).
New is our observation that the signals in the pacemaker
area differ from the surrounding area, displaying high-amplitude potentials and rapid velocity. Another refinement is the

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Fig. 7. Slow wave propagation in the distal antrum

and the proximal duodenum (A-D in Fig. 1). The
electrode array recorded slow waves from both the
canine antrum (electrodes 17) and the duodenum
(electrodes 14 17). These two regions were separated by an area of 12.5 mm wide that did not
register any electrical activity. The antral slow wave
was followed by a single spike in the distal electrodes (blue ellipse), which described a patch with a
size of 5 12.5 mm (map C). Because of the
differences in velocity, isochrones in the antrum
were drawn every second, those in the spike patch
every 200 ms, and those in the duodenum every 100
ms. The slow wave frequency in the antrum was
4.4 0.1 cycle/min and in the duodenum 17.2 1.5
cycles/min.

mode of propagation of the slow wave in the fundus itself. We

consistently observed low-amplitude fractionated propagation
in the fundus close to the greater curvature. There have been a
few studies (2, 36, 43) reporting slow wave signals in the
fundus, and we can confirm and expand that this is restricted to
the immediate vicinity of the greater curvature, at least in the
oral fundus. Careful rereading of several classics reveal early
observations of a pacemaker located in the upper part of the
stomach. Alvarez and Mahoney (1) noted that regular contractions develop in ripples which come from the neighborhood of
the cardia, a location that was supported by Bozler (5). More
recent studies have shown the existence of interstitial cells of
Cajal (ICC)-intramuscular (IM) in the fundus (9, 40). Interestingly, pathology such as diabetes or the lack of ICC may
remodel the fundus to exhibit or enhance spontaneous activity
(15, 32). We also cannot exclude that pacemaker activity could
have been unmasked by the anesthesia used. Some reports have
suggested that increasing the functional load by a Billroth II
surgery (2) or by hyperpolarizing the fundic muscle (42) might
uncover or stimulate the pacemaker activity. Furthermore, the
border between the excited and the nonexcited fundus is not

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necessarily fixed and may vary from one cycle to the next (Fig.
4). Most importantly, this fundic area of slow propagating
wave fronts links the natural pacemaker to the rest of the
stomach. Indeed, if a block occurs in this region, this will have
an immediate effect on the rhythm in the distal stomach (Fig.
8). (39).
By quantifying the conduction velocity and amplitude with
high spatial and temporal resolution, we were able to identify
in terms of electrical properties three different areas in the
stomach: 1) the fundic pacemaker area, 2) the fundus and the

corpus, and 3) the antrum. In addition, contrary to the current

prevailing view that the slow wave gradually increases in speed
as it propagates toward the antrum (18), we did not find such
an increase. Instead, as evidenced by tracings 9 10 in Fig. 3
(fundus) and tracings 8 9 in Fig. 6 (corpus to antrum), the
transition in velocity and amplitude from one area to the next
occurred abruptly, indicating the existence of a clearly demarcated border of at most a few millimeters wide. Detailed
studies have revealed the presence of several types of ICC,
amongst others ICC-Auerbachs plexus (AP) and ICC-IM in

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Fig. 8. Slow wave propagation along the ventral surface of the canine fundus, corpus, and
antrum (large electrode array in Fig. 1B).
A: 2-min tracing of 30 electrograms recorded
along the length of the stomach (locations
shown in B and C). In each case, the slow wave
was initiated in the oral part of the fundus and
propagated along the corpus and the antrum.
B: map of the slow wave indicated by the long
arrow in A. Isochrone width 5 s. The slow
wave took 45 s to reach the middle antrum
(lower part of the antrum was not mapped in
this example). C: presence of four simultaneous slow waves in the canine stomach (timing indicated by the red vertical line in A).
Each wave is plotted for durations of 6 8 s
(isochrone width 2 s). Waves a and b are
located in the fundus, wave c is located in the
corpus, while wave d is entering the antrum.
This recording also demonstrates a spontaneous block of a slow wave in the upper corpus
(red block symbol in A). This block occurred in
spite of a constant pacemaker discharge as
shown by the regular intervals plotted in the
first electrogram (values in s). The disappearance of a slow wave led to longer intervals in
the distal stomach (plotted intervals in electrogram 30).

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Fig. 9. Slow wave velocity and amplitude profile of the

canine stomach. The velocity maps and the corresponding amplitudes recorded from the fundus (F1; n 7
maps, F2; n 5 maps), the corpus (C; n 6 maps), and
the antrum (C-A; n 14 maps) were averaged along the
direction of propagation of the gastric slow wave. The
graphs show that velocity and amplitude were high in
the oral fundus, close to the pacemaker, and in the
antrum, while velocity and amplitude in the remainder
of the fundus and in the corpus was low and constant at
0.3 0.8 cm/s and 0.51.0 mV, respectively.

occur in all directions, in the longitudinal and the circumferential directions.

There are reports that support the notion of several slow
waves simultaneously present in the stomach. Cannon (6)
showed the appearance of two peristaltic waves progressing at
the same time, and this contraction pattern has been reviewed
recently (38). The fact that, on average, four slow waves are
simultaneously present on the stomach may cause problems in
interpreting the EGG. In the heart, during systole, the electrical
propagation spreads over the entire organ, followed by a period
of quiescence (diastole). The stomach, however, exhibits multiple propagating slow waves, and there are no periods of
systole or diastole. However, judging from the data presented in Fig. 8, most of the waves are located in areas that
show slow propagation and low-amplitude signals (fundus and

Fig. 10. Diagram of the gastric conduction system. The star high along the
greater curvature indicates the location of the gastric pacemaker. Dark gray
areas (pacemaker area and antrum) indicate slow wave areas with high
amplitudes and rapid velocities. Light gray areas (fundus/corpus) indicate areas
with low amplitudes and low velocities. Arrows 1 and 2 indicate oral and
circular propagation, respectively, whereas arrow 3 indicates the predominant
aboral longitudinal direction of propagation. Dashed line a-a indicates variable lines of conduction block isolating the medial fundic area. Lines b-b and
c-c indicate fixed lines of conduction block isolating antral activity from
duodenal activity.

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the stomach (8, 9, 13). The ICC-AP are thought to be responsible for the slow wave propagation in the antrum (12, 13).
Recent reports have identified ICC-IM as the dominant ICC
responsible for propagation in the corpus (11, 41). This suggests that the differences in slow wave velocity and amplitude
seen in different parts of the stomach are due to the fact that the
slow wave propagated through different types of ICC. Indeed,
Komuro (21) recently commented on the fact that the stomach,
in contrast to other gastrointestinal organs, is unique in its
spatial distribution of several types of ICCs, a fact that could be
reflected in the recorded potentials in this study. It remains to
be determined which cell type is responsible for the initiation
and propagation of the slow wave in the pacemaker area.
Propagation in the antrum (Fig. 6) is very similar to that
shown in a previous study on antral arrhythmias (28) with large
bi- or triphasic signals and rapid velocity. Slow waves always
terminated in the distal antrum, and there was a large area of
nonpropagation between the antrum and the duodenum (Fig.
7). This is similar to what has been shown in vivo (3) and in
vitro in other species (22, 44) and is caused by a regional
decrease in ICC-AP (45). Spike activity was regularly seen
in the distal antrum with propagation limited to small areas
(Fig. 7C; Refs. 23, 24) similar to what has been shown in
humans (14).
There is a crucial difference in the propagation pattern in the
intact organ and in an excised segment. In the intact stomach,
there is only one pacemaker, high up in the stomach along the
greater curvature. Propagation from this area is initially radial,
propagating both in the longitudinal and in the circumferential
direction (arrows 1 and 2 in Fig. 10). This is the same pattern
as with slow wave pacemakers in the small intestine (26,
recently reviewed in Ref. 16). Further away from the pacemaker, however, the wave front organizes itself toward the
aboral and longitudinal direction and continues to propagate as
a broad wave front until it dies out in the distal antrum (Fig. 10,
arrow 3). In other words, in the intact stomach, except for the
immediate vicinity of the pacemaker, we have not observed
any circumferential propagation. In the excised segment, however, where the connection with the natural pacemaker is
disrupted (29, 33), the spontaneous activities of local ICCs will
emerge, and propagation from those local pacemakers will

ORIGIN AND PROPAGATION OF GASTRIC SLOW WAVES

14.

15.

16.

17.
18.
19.
20.
21.
22.

23.

24.

ACKNOWLEDGMENTS

25.

We acknowledge the expert animal care provided by the staff of the

Department of Laboratory Animal Science, in particular Jef Ceulemans, Piet
Dierckx, and Leen Roefs. Dr. Brian Hrukpa is acknowledged for advice on
style and writing.

26.
27.

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corpus), and the cutaneous EGG signal may rely mostly, if not
entirely, on the larger current amplitude generated in the
antrum.
In summary, this study has identified three distinct areas
with distinct electrophysiological properties in the stomach;
two of these areas showed slow waves with high amplitude and
propagation velocity while the third area, consisting of the
fundus and the corpus, showed low slow wave amplitude and
propagation velocity. In addition, two areas were found in
which slow wave propagation did not occur at all: the first near
the esophageal junction in the fundus, close to the lesser
curvature, and the second between the distal antrum and the
duodenum. Together, these elements constitute a conduction
system (Fig. 10) that underlies the basis for the pattern of
contraction in the normal stomach (37). This knowledge of the
location and the properties of this system is also required for a
better understanding of the dysfunctional stomach, be it in the
context of gastric arrhythmias, gastroparesis, diabetes, or surgical interventions, especially in those that are now popular in
the treatment of esophageal reflex or obesitas. For example,
fundoplasty or other surgical procedures may accidentally have
repercussions on the function of the natural gastric pacemaker
or its connection to the remainder of the stomach, as was stated
many years ago (31). A better and more detailed understanding
of the gastric conduction system in the human is therefore
required to enhance the quality of treatment of these patients.

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