Colonic Activities Before Administration of Luminal
Prucalopride
HAPWs were not present at baseline nor postprandially while SPWs were
observed at baseline (n=1) and after meal intake (n=3) (Figure 1A,B). At
baseline, a pan-colonic SPW with a mean amplitude of 8.7 mmHg, maximum
pressure of 24.0 mmHg and a duration of 3.7 s was observed, not
associated with gas or liquid expulsion. After the meal, pan-colonic
SPWs were observed with an amplitude of 7.2 ± 0.8 mmHg and duration of
12.2 ± 2.5 s which entered the rectum but were not associated with gas
nor liquid expulsion (Table 1). The SPW observed at baseline was
associated with 69% relaxation of the anal sphincter while SPWs evoked
postprandially were associated with 87% relaxation. The anal sphincter
showed an intrinsic rhythmicity of 5.5 cpm (Figures 1A,B).
Effects of Intraluminal
Prucalopride on Propulsive Motor Patterns
Administration of intraluminal prucalopride in the proximal colon
introduced HAPWs and HAPW-SPWs whereas none were present during the
preceding 180 min of baseline and meal response (Figures 1C,D).
Moreover, intraluminal prucalopride resulted in a significant increase
of the SPW amplitude compared to both baseline and meal response (Table
1, Figure 2A). These effects were observed only 6 mins after
administration of intraluminal prucalopride.
During the 30 min period after prucalopride administration, six HAPWs
were generated, all belonging to category 2, that is, they started in
the ascending colon and propagated to the transverse or descending colon
with or without a change into an SPW. We have previously classified
HAPWs based on their origin and place of termination in three distinct
categories as described in Milkova et al. (37). The average amplitude of
the HAPWs was 81.5 mmHg and the average HAPW Index was 2200 mmHg.m.s.
The HAPW Index assesses the vigor with which a contraction occurs, and
it was calculated as the multiplication of average amplitude within the
20-mmHg isobar, the length of the HAPW and the duration, expressed as
mmHg.m.s. (37). The HAPWs here propagated with an average velocity of
0.53 ± 0.4 cm s-1. One HAPW was associated with urge
to defecate (Figures 2B,C & 3). Two HAPWs without SPWs, were associated
with significant, 78%, anal sphincter relaxation, lasting 26.5 ± 7 s.
Among the six HAPWs, two were HAPW-SPWs with the SPWs entering the
rectum with an average amplitude of 18.4 ± 9.8 mmHg (Table 2), they were
associated with liquid expulsion, urge to defecate and nausea (Figures
1, 2B, 3). These motor patterns were associated with 48% anal sphincter
relaxation, from 63 to 33 mmHg.
Five pan- colonic SPWs were evoked with an average amplitude of 13.0 ±
6.4 mmHg ranging between 7.3 – 24.0 mmHg with an average duration of
6.2 ± 2 s (Table 1). Vomiting associated pressure transients occurred at
the end of the recording (Figure 1).
A SPW-cluster consisting of 4 pan-colonic SPWs was associated with
significant anal sphincter relaxation. Anal sphincter did not recover in
between the four SPWs. Before relaxation, the mean amplitude of the
sphincter was 31.6 mmHg with maximum and minimum amplitudes of 56.0 and
15.4 mmHg respectively. During the relaxation phase, the anal sphincter
amplitude decreased to 13.1 mmHg with maximum pressure of 45 and minimum
pressure of 3.6 mmHg resulting in 60% relaxation (Table 2). One pan
colonic SPW overlapped with an HAPW; therefore, anal sphincter
relaxation could not be reliably attributed to either of the motor
patterns.
The degree of relaxation associated with SPWs during baseline, meal and
intraluminal prucalopride did not show any significant difference.